Updated on 2024/10/01

Information

 

写真a

 
BABA YOSHIHIRO
 
Organization
Medical Institute of Bioregulation Department of Immunobiology and Neuroscience Professor
Medical Institute of Bioregulation （Joint Appointment）
Graduate School of Medical Sciences Department of Medicine（Joint Appointment）
Graduate School of Medical Sciences Department of Medical Sciences（Joint Appointment）
School of Dentistry Department of Dentistry（Joint Appointment）
Title
Professor
Contact information
メールアドレス
Tel
0926426838
Profile
生体防御医学研究所分子機能制御部門において免疫ゲノム生物学分野を主宰している。免疫機構センターを兼任。免疫細胞機能解析と疾患制御の研究教育活動を行なっている。また、生体防御医学研究所・発生工学実験室室長としてマウス飼育室の管理、遺伝子改変マウス作成業務を担当している。
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External link

Degree

  • Ph.D.

Research Interests・Research Keywords

  • Research theme：Understanding of B cell development and functions

    Keyword：B cells, antibody, plasma cells, plasmablast, germinal center, memory B cells, IL-10, genetically modified mice

    Research period： 2017.4

  • Research theme：Elucidation of the mechanism how B cells regulate disorders

    Keyword：regulatory B cells, autoimmune disease, allergy, inflammation, cancer, infection, transplantation, cytokine, repertoire, human B cell

    Research period： 2017.4

Awards

  • 第6回日本免疫学会研究奨励賞受賞

    2011.11   日本免疫学会  

Papers

  • BCR signaling in germinal center B cell selection

    Inoue, T; Baba, Y; Kurosaki, T

    TRENDS IN IMMUNOLOGY   45 ( 9 )   693 - 704   2024.9   （ ISSN:1471-4906 eISSN:1471-4981 ）

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    Language：English   Publisher：Trends in Immunology  

    When mature B cells are activated by antigens, the selection of these activated B cells takes place particularly during T cell-dependent immune responses in which an improved antibody repertoire is generated through somatic hypermutation in germinal centers (GCs). In this process the importance of antigen presentation by GC B cells, and subsequent T follicular helper (Tfh) cell help in positive selection of GC B cells, has been well appreciated. By contrast, the role of B cell receptor (BCR) signaling per se remains unclear. Strong experimental support for the involvement of BCR signaling in GC B cell selection has now been provided. Interestingly, these studies suggest that several checkpoints operating through the BCR ensure affinity maturation.

    DOI： 10.1016/j.it.2024.07.005

    Web of Science

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  • Plasma cell differentiation is regulated by the expression of histone variant H3.3

    Saito, Y; Harada, A; Ushijima, M; Tanaka, K; Higuchi, R; Baba, A; Murakami, D; Nutt, SL; Nakagawa, T; Ohkawa, Y; Baba, Y

    NATURE COMMUNICATIONS   15 ( 1 )   5004   2024.6   （ eISSN:2041-1723 ）

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    Language：English   Publisher：Nature Communications  

    The differentiation of B cells into plasma cells is associated with substantial transcriptional and epigenetic remodeling. H3.3 histone variant marks active chromatin via replication-independent nucleosome assembly. However, its role in plasma cell development remains elusive. Herein, we show that during plasma cell differentiation, H3.3 is downregulated, and the deposition of H3.3 and chromatin accessibility are dynamically changed. Blockade of H3.3 downregulation by enforced H3.3 expression impairs plasma cell differentiation in an H3.3-specific sequence-dependent manner. Mechanistically, enforced H3.3 expression inhibits the upregulation of plasma cell-associated genes such as Irf4, Prdm1, and Xbp1 and maintains the expression of B cell-associated genes, Pax5, Bach2, and Bcl6. Concomitantly, sustained H3.3 expression prevents the structure of chromatin accessibility characteristic for plasma cells. Our findings suggest that appropriate H3.3 expression and deposition control plasma cell differentiation.

    DOI： 10.1038/s41467-024-49375-x

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  • Humoral responses are enhanced by facilitating B cell viability by Fcrl5 overexpression in B cells

    Ono, C; Kochi, Y; Baba, Y; Tanaka, S

    INTERNATIONAL IMMUNOLOGY   36 ( 10 )   529 - 540   2024.6   （ ISSN:0953-8178 eISSN:1460-2377 ）

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    Language：English   Publisher：International Immunology  

    B cell initial activity is regulated through a balance of activation and suppression mediated by regulatory molecules expressed in B cells; however, the molecular mechanisms underlying this process remain incompletely understood. In this study, we investigated the function of the Fc receptor-like (Fcrl) family molecule Fcrl5, which is constitutively expressed in naive B cells, in humoral immune responses. Our study demonstrated that B cell-specific overexpression of Fcrl5 enhanced antibody (Ab) production in both T cell-independent type 1 (TI1) and T cell-dependent (TD) responses. Additionally, it promoted effector B cell formation under competitive conditions in TD responses. Mechanistically, in vitro ligation of Fcrl5 by agonistic Abs reduced cell death and enhanced proliferation in lipopolysaccharide-stimulated B cells. In the presence of anti-CD40 Abs and IL-5, the Fcrl5 ligation not only suppressed cell death but also enhanced differentiation into plasma cells. These findings reveal a novel role of Fcrl5 in promoting humoral immune responses by enhancing B cell viability and plasma cell differentiation.

    DOI： 10.1093/intimm/dxae028

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  • Exploratory mass cytometry analysis reveals immunophenotypes of cancer treatment-related pneumonitis

    Yanagihara, T; Hata, K; Matsubara, K; Kunimura, K; Suzuki, K; Tsubouchi, K; Ikegame, S; Baba, Y; Fukui, Y; Okamoto, I

    ELIFE   12   2024.4   （ ISSN:2050-084X ）

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    Language：English   Publisher：eLife  

    Anticancer treatments can result in various adverse effects, including infections due to immune suppression/dysregulation and drug-induced toxicity in the lung. One of the major opportunistic infections is Pneumocystis jirovecii pneumonia (PCP), which can cause severe respiratory complications and high mortality rates. Cytotoxic drugs and immune-checkpoint inhibitors (ICIs) can induce interstitial lung diseases (ILDs). Nonetheless, the differentiation of these diseases can be difficult, and the pathogenic mechanisms of such diseases are not yet fully understood. To better comprehend the immunophenotypes, we conducted an exploratory mass cytometry analysis of immune cell subsets in bronchoalveolar lavage fluid from patients with PCP, cytotoxic drug-induced ILD (DI-ILD), and ICI-associated ILD (ICI-ILD) using two panels containing 64 markers. In PCP, we observed an expansion of the CD16+ T cell population, with the highest CD16+ T proportion in a fatal case. In ICI-ILD, we found an increase in CD57+ CD8+ T cells expressing immune checkpoints (TIGIT+ LAG3+ TIM-3+ PD-1+), FCRL5+ B cells, and CCR2+ CCR5+ CD14+ monocytes. These findings uncover the diverse immunophenotypes and possible pathomechanisms of cancer treatment-related pneumonitis.

    DOI： 10.7554/eLife.87288

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  • Bruton's tyrosine kinase inhibition limits endotoxic shock by suppressing IL-6 production by marginal zone B cells in mice

    Kawata, K; Hatano, S; Baba, A; Imabayashi, K; Baba, Y

    FRONTIERS IN IMMUNOLOGY   15   1388947   2024.4   （ ISSN:1664-3224 ）

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    Language：English   Publisher：Frontiers in Immunology  

    Sepsis is a systemic inflammatory response to a severe, life-threatening infection with organ dysfunction. Although there is no effective treatment for this fatal illness, a deeper understanding of the pathophysiological basis of sepsis and its underlying mechanisms could lead to the development of new treatment approaches. Here, we demonstrate that the selective Bruton’s tyrosine kinase (Btk) inhibitor acalabrutinib augments survival rates in a lipopolysaccharide (LPS)-induced septic model. Our in vitro and in vivo findings both indicate that acalabrutinib reduces IL-6 production specifically in marginal zone B (MZ B) cells rather than in macrophages. Furthermore, Btk-deficient MZ B cells exhibited suppressed LPS-induced IL-6 production in vitro. Nuclear factor-kappa B (NF-κB) signaling, which is the downstream signaling cascade of Toll-like receptor 4 (TLR4), was also severely attenuated in Btk-deficient MZ B cells. These findings suggest that Btk blockade may prevent sepsis by inhibiting IL-6 production in MZ B cells. In addition, although Btk inhibition may adversely affect B cell maturation and humoral immunity, antibody responses were not impaired when acalabrutinib was administered for a short period after immunization with T-cell-independent (TI) and T-cell-dependent (TD) antigens. In contrast, long-term administration of acalabrutinib slightly impaired humoral immunity. Therefore, these findings suggest that Btk inhibitors may be a potential option for alleviating endotoxic shock without compromising humoral immunity and emphasize the importance of maintaining a delicate balance between immunomodulation and inflammation suppression.

    DOI： 10.3389/fimmu.2024.1388947

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  • Type I interferon promotes the fate of Toll-like receptor 9-stimulated follicular B cells to plasma cell differentiation

    Higuchi, R; Tanaka, K; Saito, Y; Murakami, D; Nakagawa, T; Nutt, SL; Ohkawa, Y; Baba, Y

    PNAS NEXUS   3 ( 4 )   pgae152   2024.3   （ eISSN:2752-6542 ）

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    Language：English   Publisher：PNAS Nexus  

    The activation and differentiation of B cells into plasma cells (PCs) play critical roles in the immune response to infections and autoimmune diseases. Toll-like receptor 9 (TLR9) responds to bacterial and viral DNA containing unmethylated CpG motifs and triggers immune responses in B cells; however, abnormal recognition of self-DNA by TLR9 can cause autoimmune diseases. When stimulated with TLR9 agonists, follicular (FO) B cells, a subset of B cells residing in the FO regions of secondary lymphoid organs, exhibit a propensity for activation but fail to give rise to PCs. The factors that enable the transition of TLR9-activated FO B cells from activation to differentiation into PCs remain unclear. In this study, we show that type I interferon-alpha (IFNα) signaling causes FO B cells activated by CpG stimulation to differentiate into PCs. Although CpG stimulation alone only temporarily increased interferon regulatory factor 4 (IRF4) expression in FO B cells, co-stimulation with both CpG and IFNα enhanced and maintained high IRF4 expression levels, ultimately enabling the cells to differentiate into PCs. Overexpression of IRF4 in FO B cells results in CpG-induced PC transition without IFN signaling. Furthermore, co-stimulation of TLR9 and IFNα receptors significantly enhanced mammalian target of rapamycin (mTOR) signaling, which regulates IRF4 expression and PC generation. These findings suggest that IFNα may play a key role in promoting the fate of PC differentiation in FO B cells activated by TLR9 stimulation.

    DOI： 10.1093/pnasnexus/pgae152

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  • STIM-mediated calcium influx regulates maintenance and selection of germinal center B cells. Invited Reviewed International journal

    Yada Y, Matsumoto M, Inoue T, Baba A, Higuchi R, Kawai C, Yanagisawa M, Kitamura D, Ohga S, Kurosaki T, Baba Y.

    J. Exp. Med.   2024.1

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    Language：English   Publishing type：Research paper (scientific journal)  

  • Regulation mechanisms of CARMA1–Bcl10–MALT1 complex assembly inferred from the analysis of TRAF6-deficient cells Invited Reviewed International journal

    2023.12

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    Language：English   Publishing type：Research paper (scientific journal)  

  • Upregulated Fcrl5 disrupts B cell anergy and causes autoimmune disease. Invited Reviewed International journal

    Ono C, Tanaka S, Myouzen K, Iwasaki T, Ueda M, Oda Y, Yamamoto K, Kochi Y, Baba Y.

    Front. Immunol.   2023.12

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    Language：English   Publishing type：Research paper (scientific journal)  

  • Mass cytometry analysis of B-cell populations in extranodal marginal-zone lymphoma of mucosa-associated lymphoid tissue of the lung

    Yanagihara, T; Hata, K; Matsubara, K; Kunimura, K; Suzuki, K; Tsubouchi, K; Ikegame, S; Baba, Y; Fukui, Y; Okamoto, I

    ANNALS OF HEMATOLOGY   102 ( 10 )   2959 - 2961   2023.10   （ ISSN:0939-5555 eISSN:1432-0584 ）

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    Language：English   Publisher：Annals of Hematology  

    DOI： 10.1007/s00277-023-05391-3

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  • Cardiac Autoantibodies Against Cardiac Troponin I in Post-Myocardial Infarction Heart Failure: Evaluation in a Novel Murine Model and Applications in Therapeutics

    Furusawa, S; Ikeda, M; Ide, T; Kanamura, T; Miyamoto, HD; Abe, K; Ishimaru, K; Watanabe, M; Tsutsui, Y; Miyake, R; Fujita, S; Tohyama, T; Matsushima, S; Baba, Y; Tsutsui, H

    CIRCULATION-HEART FAILURE   16 ( 10 )   895 - 908   2023.10   （ ISSN:1941-3289 eISSN:1941-3297 ）

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    Language：English   Publisher：Circulation: Heart Failure  

    BACKGROUND: Cardiac autoantibodies (cAAbs) are involved in the progression of adverse cardiac remodeling in heart failure (HF). However, our understanding of cAAbs in HF is limited owing to the absence of relevant animal models. Herein, we aimed to establish and characterize a murine model of cAAb-positive HF after myocardial infarction (MI), thereby facilitating the development of therapeutics targeting cAAbs in post-MI HF. METHODS: MI was induced in BALB/c mice. Plasma cAAbs were evaluated using modified Western blot-based methods. Prognosis, cardiac function, inflammation, and fibrosis were compared between cAAb-positive and cAAb-negative MI mice. Rapamycin was used to inhibit cAAb production. RESULTS: Common cAAbs in BALB/c MI mice targeted cTnI (cardiac troponin I). Herein, 71% (24/34) and 44% (12/27) of the male and female MI mice, respectively, were positive for cAAbs against cTnI (cTnIAAb). Germinal centers were formed in the spleens and mediastinal lymph nodes of cTnIAAb-positive MI mice. cTnIAAb-positive MI mice showed progressive cardiac remodeling with a worse prognosis (P=0.014, by log-rank test), which was accompanied by cardiac inflammation, compared with that in cTnIAAb-negative MI mice. Rapamycin treatment during the first 7 days after MI suppressed cTnIAAb production (cTnIAAb positivity, 59% [29/49] and 7% [2/28] in MI mice treated with vehicle and rapamycin, respectively; P<0.001, by Pearson χ2 test), consequently improving the survival and ameliorating cardiac inflammation, cardiac remodeling, and HF in MI mice. CONCLUSIONS: The present post-MI HF model may accelerate our understanding of cTnIAAb and support the development of therapeutics against cTnIAAbs in post-MI HF.

    DOI： 10.1161/CIRCHEARTFAILURE.122.010347

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  • Upregulated Fcrl5 disrupts B cell anergy causes autoimmune disease

    Ono, C; Tanaka, S; Myouzen, K; Iwasaki, T; Ueda, M; Oda, Y; Yamamoto, K; Kochi, Y; Baba, Y

    FRONTIERS IN IMMUNOLOGY   14   1276014   2023.9   （ ISSN:1664-3224 ）

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    Language：English   Publisher：Frontiers in Immunology  

    B cell anergy plays a critical role in maintaining self-tolerance by inhibiting autoreactive B cell activation to prevent autoimmune diseases. Here, we demonstrated that Fc receptor-like 5 (Fcrl5) upregulation contributes to autoimmune disease pathogenesis by disrupting B cell anergy. Fcrl5—a gene whose homologs are associated with human autoimmune diseases—is highly expressed in age/autoimmunity-associated B cells (ABCs), an autoreactive B cell subset. By generating B cell-specific Fcrl5 transgenic mice, we demonstrated that Fcrl5 overexpression in B cells caused systemic autoimmunity with age. Additionally, Fcrl5 upregulation in B cells exacerbated the systemic lupus erythematosus-like disease model. Furthermore, an increase in Fcrl5 expression broke B cell anergy and facilitated toll-like receptor signaling. Thus, Fcrl5 is a potential regulator of B cell-mediated autoimmunity by regulating B cell anergy. This study provides important insights into the role of Fcrl5 in breaking B cell anergy and its effect on the pathogenesis of autoimmune diseases.

    DOI： 10.3389/fimmu.2023.1276014

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  • Regulation mechanisms of CARMA1-Bcl10-MALT1 complex assembly inferred from the analysis of TRAF6-deficient cells

    Inoue, K; Yasuda, T; Baba, Y; Yamamoto, T; Kurosaki, T; Shinohara, H

    GENES TO CELLS   28 ( 6 )   411 - 421   2023.6   （ ISSN:1356-9597 eISSN:1365-2443 ）

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    Language：English   Publisher：Genes to Cells  

    The CARMA1–Bcl10–MALT1 (CBM) signalosome is a crucial module of NF-κB activation in B cell receptor (BCR) signaling. Biophysical studies have shown that the E3 ubiquitin ligase TRAF6 cooperatively modifies the CBM signalosome; however, the specific details regarding how TRAF6 is involved in BCR signal-induced CBM formation remain unclear. In this study, we aimed to reveal the influences of TRAF6 on CBM formation and TAK1 and IKK activities using DT40 B cells which lack all the exons of TRAF6. In TRAF6-null cells we found: (i) attenuation of TAK1 activity and abolishment of IKK activity and (ii) sustained binding of CARMA1 to Bcl10. To account for the molecular mechanism causing these dynamics, we performed a mathematical model analysis. The mathematical model analysis showed that the regulation of IKK activation by TRAF6 can reproduce TAK1 and IKK activities in TRAF6 null cells, and that the TRAF6 related signal-dependent inhibitor suppresses CARMA1 binding to Bcl10 in wild-type cells. These results suggest that TRAF6 contributes to the positive regulation of IKK activation via TAK1, alongside the negative signal-dependent regulation of CARMA1 binding to Bcl10.

    DOI： 10.1111/gtc.13022

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  • Mass cytometry identifies characteristic immune cell subsets in bronchoalveolar lavage fluid from interstitial lung diseases

    Hata, K; Yanagihara, T; Matsubara, K; Kunimura, K; Suzuki, K; Tsubouchi, K; Eto, D; Ando, H; Uehara, M; Ikegame, S; Baba, Y; Fukui, Y; Okamoto, I

    FRONTIERS IN IMMUNOLOGY   14   1145814   2023.3   （ ISSN:1664-3224 ）

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    Language：English   Publisher：Frontiers in Immunology  

    Immune cells have been implicated in interstitial lung diseases (ILDs), although their phenotypes and effector mechanisms remain poorly understood. To better understand these cells, we conducted an exploratory mass cytometry analysis of immune cell subsets in bronchoalveolar lavage fluid (BALF) from patients with idiopathic pulmonary fibrosis (IPF), connective-tissue disease (CTD)-related ILD, and sarcoidosis, using two panels including 64 markers. Among myeloid cells, we observed the expansion of CD14+ CD36hi CD84hiCCR2– monocyte populations in IPF. These CD14+ CD36hi CD84hi CCR2– subsets were also increased in ILDs with a progressive phenotype, particularly in a case of acute exacerbation (AEx) of IPF. Analysis of B cells revealed the presence of cells at various stages of differentiation in BALF, with a higher percentage of IgG memory B cells in CTD-ILDs and a trend toward more FCRL5+ B cells. These FCRL5+ B cells were also present in the patient with AEx-IPF and sarcoidosis with advanced lung lesions. Among T cells, we found increased levels of IL-2R+ TIGIT+ LAG3+ CD4+ T cells in IPF, increased levels of CXCR3+ CD226+ CD4+ T cells in sarcoidosis, and increased levels of PD1+ TIGIT+ CD57+ CD8+ T cells in CTD-ILDs. Together, these findings underscore the diverse immunopathogenesis of ILDs.

    DOI： 10.3389/fimmu.2023.1145814

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  • MHC class II inhibits the generation of IL-17A<SUP>+</SUP> Vγ6 γδ T cells in the thymus at perinatal stage

    Hatano, S; Mine, K; Noguchi, N; Matsumoto, M; Baba, Y; Yoshikai, Y

    EUROPEAN JOURNAL OF IMMUNOLOGY   52 ( 8 )   1366 - 1368   2022.8   （ ISSN:0014-2980 eISSN:1521-4141 ）

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    Language：English   Publisher：European Journal of Immunology  

    DOI： 10.1002/eji.202149542

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  • Pyruvate enhances oral tolerance via GPR31

    Liu, QZ; Umemoto, E; Morita, N; Kayama, H; Baba, Y; Kurosaki, T; Okumura, R; Takeda, K

    INTERNATIONAL IMMUNOLOGY   34 ( 7 )   343 - 352   2022.7   （ ISSN:0953-8178 eISSN:1460-2377 ）

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    Language：English   Publisher：International Immunology  

    CX3CR1high myeloid cells in the small intestine mediate the induction of oral tolerance by driving regulatory T (Treg) cells. Bacterial metabolites, e.g. pyruvate and lactate, induce a dendrite extension of CX3CR1high myeloid cells into the intestinal lumen via GPR31. However, it remains unclear whether the pyruvate-GPR31 axis is involved in the induction of oral tolerance. Here, we show that pyruvate enhances oral tolerance in a GPR31-dependent manner. In ovalbumin (OVA)-fed Gpr31-deficient mice, an OVA-induced delayed-type hypersensitivity response was substantially induced, demonstrating the defective induction of oral tolerance in Gpr31-deficient mice. The percentage of RORγt+ Treg cells in the small intestine was reduced in Gpr31-deficient mice. In pyruvate-treated wild-type mice, a low dose of OVA efficiently induced oral tolerance. IL-10 production from intestinal CX3CR1high myeloid cells was increased by OVA ingestion in wild-type mice, but not in Gpr31-deficient mice. CX3CR1high myeloid cell-specific IL-10-deficient mice showed a defective induction of oral tolerance to OVA and a decreased accumulation of OVA-specific Treg cells in the small intestine. These findings demonstrate that pyruvate enhances oral tolerance through a GPR31-dependent effect on intestinal CX3CR1high myeloid cells.

    DOI： 10.1093/intimm/dxac010

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  • Quiescent B Cells Acquire Sensitivity to Cell Cycle Arresting Agents by B Cell Receptor Stimulation

    Hosokawa, T; Tanaka, S; Mori, T; Baba, Y; Katayama, Y

    BIOLOGICAL & PHARMACEUTICAL BULLETIN   45 ( 7 )   847 - 850   2022.7   （ ISSN:0918-6158 eISSN:1347-5215 ）

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  • Efficient human-like antibody repertoire and hybridoma production in trans-chromosomic mice carrying megabase-sized human immunoglobulin loci. Invited Reviewed International journal

    Satofuka H, Abe S, Moriwaki T, Okada A, Kazuki K, Tanaka H, Yamazaki K, Hichiwa G, Morimoto K, Takayama H, Nakayama Y, Hatano S, Yada Y, Murakami Y, Baba Y, Oshimura M, Tomizuka K, Kazuki Y.

    Nat. Commun.   2022.6

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    Language：Japanese   Publishing type：Research paper (scientific journal)  

  • Special AT-rich sequence-binding protein 1 supports survival of naïve B cells stimulated by B cell receptors. Invited Reviewed International journal

    2022.6

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  • Silencing and activating anergic B cells. Reviewed International journal

    Shinya Tanaka, Wataru Ise, Yoshihiro Baba, Tomohiro Kurosaki

    Immunol Rev   307 ( 1 )   43 - 52   2022.5

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1111/imr.13053.

  • ER membrane protein complex 1 interacts with STIM1 and regulates store-operated Ca2+ entry. Reviewed International journal

    Kazuhiko Kawata, Akemi Baba, Masayuki Shiota, Hideki Wanibuchi, Yoshihiro Baba

    J Biochem   170 ( 4 )   483 - 488   2021.12

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    DOI： J Biochem .

  • Generation and characterization of CD19-iCre mice as a tool for efficient and specific conditional gene targeting in B cells. Reviewed International journal

    Tomoharu Yasuda, Yuichi Saito, Chisato Ono, Kazuhiko Kawata, Akemi Baba, Yoshihiro Baba

    Sci Rep   11 ( 1 )   5524 - 5524   2021.3

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    DOI： 10.1038/s41598-021-84786-6.

  • Tet2 and Tet3 in B cells are required to repress CD86 and prevent autoimmunity Reviewed International journal

    Tanaka S, Ise W, Inoue T, Ito A, Ono C, Shima Y, Sakakibara S, Nakayama M, Fujii K, Miura I, Sharif J, Koseki H, Koni PA, Raman I, Li QZ, Kubo M, Fujiki K, Nakato R, Shirahige K, Araki H, Miura F, Ito T, Kawakami E, Baba Y, Kurosaki T.

    Nat Immunol.   21 ( 8 )   950 - 961   2020.8

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    DOI： 10.1038/s41590-020-0700-y.

  • TRPM5 Negatively Regulates Calcium-Dependent Responses in Lipopolysaccharide-Stimulated B Lymphocytes Reviewed International journal

    Taiki Sakaguchi, Ryu Okumura, Chisato Ono, Daisuke Okuzaki, Takafumi Kawai, Yoshifumi Okochi, Natsuko Tanimura, Mari Murakami, Hisako Kayama, Eiji Umemoto, Hidetaka Kioka, Tomohito Ohtani, Yasushi Sakata, Kensuke Miyake, Yasushi Okamura, Yoshihiro Baba, Kiyoshi Takeda

    Cell Rep   31 ( 10 )   107755 - 107755   2020.6

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    DOI： 10.1016/j.celrep.2020.107755.

  • B Cell Receptor Signaling. Reviewed International journal

    Sinya Tanaka, Yoshihiro Baba.

    Adv Exp Med Biol   1254   23 - 36   2020.4

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    DOI： 10.1007/978-981-15-3532-1_2.

  • GPR40 activation initiates store-operated Ca2+ entry and potentiates insulin secretion via the IP3R1/STIM1/Orai1 pathway in pancreatic β-cells Reviewed

    9 ( 1 )   2019.12

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    The long-chain fatty acid receptor GPR40 plays an important role in potentiation of glucose-induced insulin secretion (GIIS) from pancreatic β-cells. Previous studies demonstrated that GPR40 activation enhances Ca2+ release from the endoplasmic reticulum (ER) by activating inositol 1,4,5-triphosphate (IP3) receptors. However, it remains unknown how ER Ca2+ release via the IP3 receptor is linked to GIIS potentiation. Recently, stromal interaction molecule (STIM) 1 was identified as a key regulator of store-operated Ca2+ entry (SOCE), but little is known about its contribution in GPR40 signaling. We show that GPR40-mediated potentiation of GIIS is abolished by knockdown of IP3 receptor 1 (IP3R1), STIM1 or Ca2+-channel Orai1 in insulin-secreting MIN6 cells. STIM1 and Orai1 knockdown significantly impaired SOCE and the increase of intracellular Ca2+ by the GPR40 agonist, fasiglifam. Furthermore, β-cell-specific STIM1 knockout mice showed impaired fasiglifam-mediated GIIS potentiation not only in isolated islets but also in vivo. These results indicate that the IP3R1/STIM1/Orai1 pathway plays an important role in GPR40-mediated SOCE initiation and GIIS potentiation in pancreatic β-cells.

    DOI： 10.1038/s41598-019-52048-1

  • Heterogeneous subsets of B-lineage regulatory cells (Breg cells) Reviewed

    Yoshihiro Baba, Yuichi Saito, Yasuaki Kotetsu

    International immunology   32 ( 3 )   155 - 162   2019.12

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1093/intimm/dxz068

  • The COMMD3/8 complex determines GRK6 specificity for chemoattractant receptors Reviewed

    Akiko Nakai, Jun Fujimoto, Haruhiko Miyata, Ralf Stumm, Masashi Narazaki, Stefan Schulz, Yoshihiro Baba, Atsushi Kumanogoh, Kazuhiro Suzuki

    Journal of Experimental Medicine   216 ( 7 )   1630 - 1647   2019.1

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1084/jem.20181494

  • Sensitive detection of fluorescence in western blotting by merging images Reviewed

    Yukari Kondo, Shinichiro Higa, Takeshi Iwasaki, Tomoya Matsumoto, Kazumitsu Maehara, Akihito Harada, Yoshihiro Baba, Masatoshi Fujita, Yasuyuki Ohkawa

    PloS one   13 ( 1 )   2018.1

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1371/journal.pone.0191532

  • Stromal interaction molecule 1 haploinsufficiency causes maladaptive response to pressure overload Reviewed

    Takayoshi Ohba, Hiroyuki Watanabe, Manabu Murakami, Kenji Iino, Takeshi Adachi, Yoshihiro Baba, Tomohiro Kurosaki, Kyoichi Ono, Hiroshi Ito

    PloS one   12 ( 11 )   2017.11

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1371/journal.pone.0187950

  • UDP-induced phagocytosis and ATP-stimulated chemotactic migration are impaired in STIM1 -/- microglia in vitro and in vivo Reviewed

    Hye Min Lim, Heo Woon, Jung Woo Han, Yoshihiro Baba, Tomohiro Kurosaki, Min Goo Lee, Joo Young Kim

    Mediators of Inflammation   2017   2017.1

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1155/2017/8158514

  • The activated conformation of integrin β7 is a novel multiple myeloma-specific target for CAR T cell therapy Reviewed

    23 ( 12 )   1436 - 1443   2017.1

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    Cancer-specific cell-surface antigens are ideal targets for monoclonal antibody (mAb)-based immunotherapy but are likely to have previously been identified in transcriptome or proteome analyses. Here, we show that the active conformer of an integrin can serve as a specific therapeutic target for multiple myeloma (MM). We screened >10,000 anti-MM mAb clones and identified MMG49 as an MM-specific mAb specifically recognizing a subset of integrin β77 molecules. The MMG49 epitope, in the N-terminal region of the β77 chain, is predicted to be inaccessible in the resting integrin conformer but exposed in the active conformation. Elevated expression and constitutive activation of integrin β77 conferred high MMG49 reactivity on MM cells, whereas MMG49 binding was scarcely detectable in other cell types including normal integrin β77 + lymphocytes. T cells transduced with MMG49-derived chimeric antigen receptor (CAR) exerted anti-MM effects without damaging normal hematopoietic cells. Thus, MMG49 CAR T cell therapy is promising for MM, and a receptor protein with a rare but physiologically relevant conformation can serve as a cancer immunotherapy target.

    DOI： 10.1038/nm.4431

  • LRRK1 is critical in the regulation of B-cell responses and CARMA1-dependent NF-κB activation Reviewed

    6   2016.5

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    B-cell receptor (BCR) signaling plays a critical role in B-cell activation and humoral immunity. In this study, we discovered a critical function of leucine-rich repeat kinase 1 (LRRK1) in BCR-mediated immune responses. Lrrk1 mice exhibited altered B1a-cell development and basal immunoglobulin production. In addition, these mice failed to produce IgG3 antibody in response to T cell-independent type 2 antigen due to defects in IgG3 class-switch recombination. Concomitantly, B cells lacking LRRK1 exhibited a profound defect in proliferation and survival upon BCR stimulation, which correlated with impaired BCR-mediated NF-κB activation and reduced expression of NF-κB target genes including Bcl-x L, cyclin D2, and NFATc1/αA. Furthermore, LRRK1 physically interacted and potently synergized with CARMA1 to enhance NF-κB activation. Our results reveal a critical role of LRRK1 in NF-κB signaling in B cells and the humoral immune response.

    DOI： 10.1038/srep25738

  • Sialylation converts arthritogenic IgG into inhibitors of collagen-induced arthritis Invited Reviewed International journal

    Yusuke Ohmi, Wataru Ise, AkiraHarazono, Daisuke Takakura, Hidehiro Fukuyama, Yoshihiro Baba, Masahi Narazaki, Hirofumi, Shoda, Nobunori Takahashi, Yuki Ohkawa, Shuting Ji, Fumihiro Sugiyama, Keishi Fujio, Atsuhi Kumanogoh, Kazuhiko Yamamoto, Nana Kawasaki, Tomohiro Kurosaki, Yoshimasa Takahashi, Koichi Furukawa.

    NATURE COMMUNICATIONS   7   11205   2016.4

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1038/ncomms11205

  • Cytokine Regulation of B Cell Activation and Differentiation

    Yoshihiro Baba, Barry Ripley, Tadamitsu Kishimoto, Tomohiro Kurosaki

    Activation of the Immune System   3   244 - 252   2016.4

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    Language：English  

    DOI： 10.1016/B978-0-12-374279-7.09017-2

  • Role of Calcium Signaling in B Cell Activation and Biology Invited Reviewed International journal

    Yoshihiro Baba, Tomohiro Kurosaki

    Curr. Top. Microbiol. Immunol.   393   143 - 174   2015.9

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1007/82_2015_477

  • Ca2+ signals regulate mitochondrial metabolism by stimulating CREB-mediated expression of the mitochondrial Ca2+ uniporter gene MCU Reviewed

    Santhanam Shanmughapriya, Sudarsan Rajan, Nicholas E. Hoffman, Xueqian Zhang, Shuchi Guo, Jill E. Kolesar, Kevin J. Hines, Jonathan Ragheb, Neelakshi R. Jog, Roberto Caricchio, Yoshihiro Baba, Yandong Zhou, Brett A. Kaufman, Joseph Y. Cheung, Tomohiro Kurosaki, Donald L. Gill, Muniswamy Madesh

    Science Signaling   8 ( 366 )   ra23   2015.3

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1126/scisignal.2005673

  • Signals controlling the development and activity of regulatory B-lineage cells Reviewed

    Yoshihiro Baba, Masanori Matsumoto, Tomohiro Kurosaki

    International Immunology   27 ( 10 )   487 - 493   2015.1

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1093/intimm/dxv027

  • Interleukin-10-Producing Plasmablasts Exert Regulatory Function in Autoimmune Inflammation Invited Reviewed International journal

    Masanori Matsumoto, Akemi Baba, Takafumi Yokota, Hiroyoshi Nishikawa, Yasuyuki Ohkawa, Hisako Kayama, Axel Kallies, Stephen L Nutt, Shimon Sakaguchi, Kiyoshi Takeda, Tomohiro Kurosaki, Yoshihiro Baba

    IMMUNITY   41 ( 6 )   1040 - 1051   2014.12

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1016/j.immuni.2014.10.016

  • Calcium signaling in B cells Regulation of cytosolic Ca2+ increase and its sensor molecules, STIM1 and STIM2 Reviewed

    Yoshihiro Baba, Masanori Matsumoto, Tomohiro Kurosaki

    Molecular Immunology   62 ( 2 )   339 - 343   2014.12

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1016/j.molimm.2013.10.006

  • Potent functional uncoupling between STIM1 and Orai1 by dimeric 2-aminodiphenyl borinate analogs Invited Reviewed International journal

    Eunan Hendron, Xizhuo Wang, Yandong Zhou, Xiangyu Cai, Jun-ichi Goto, Katsuhiko Mikoshiba, Yoshihiro Baba, Tomohiro Kurosaki, Youjun Wang, Donald L Gill.

    CELL CALCIUM   56 ( 6 )   482 - 492   2014.12

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1016/j.ceca.2014.10.005

  • Intrinsic disorder mediates cooperative signal transduction in STIM1 Reviewed

    Yukio Furukawa, Shunsuke Teraguchi, Takahisa Ikegami, Onur Dagliyan, Lin Jin, Damien Hall, Nikolay V. Dokholyan, Keiichi Namba, Shizuo Akira, Tomohiro Kurosaki, Yoshihiro Baba, Daron M. Standley

    Journal of Molecular Biology   426 ( 10 )   2082 - 2097   2014.5

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1016/j.jmb.2014.03.006

  • STIM1 Controls Neuronal Ca2+ Signaling, mGluR1-Dependent Synaptic Transmission, and Cerebellar Motor Behavior Reviewed

    Neuron   82 ( 3 )   635 - 644   2014.5

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1016/j.neuron.2014.03.027

  • Generation of colonic IgA-secreting cells in the caecal patch Invited Reviewed International journal

    Kazunori Masahara, Eiji Umemoto, Hisako Kayama, Manato Kotani, Shota Nakamura, Takashi Kurakawa, Junichi Kikuta, Kazuyoshi Gotoh, Daisuke Motooka, Shintaro Sato, Tomonori Higuchi, Yoshihiro Baba, Tomohiro Kurosaki, Makoto Kinoshita, Youke Shimada, Taishi Kimura, Ryu Okumura, Akira Takeda, Masaru Tajima, Osamu YOshie, Masahiro Fukukazaa, Hiroshi Kiyono, Sidonia Fagarasan, Tetsuya Iida, Masaru Ishii, Kiyoshi Takeda.

    NATURE COMMUNICATIONS   5   2014.4

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1038/ncomms4704

  • STIM1 calcium sensor is required for activation of the phagocyte oxidase during in flammation and host defense Reviewed

    Hong Zhang, Regina A. Clemens, Fengchun Liu, Yongmei Hu, Yoshihiro Baba, Pierre Theodore, Tomohiro Kurosaki, Clifford A. Lowell

    Blood   123 ( 14 )   2238 - 2249   2014.4

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1182/blood-2012-08-450403

  • Role of STIM-dependent Ca2+ influx in regulatory B cells Reviewed

    Masanori Matsumoto, Yoshihiro Baba

    Yakugaku Zasshi   133 ( 4 )   419 - 425   2013.4

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1248/yakushi.12-00227-2

  • Surf4 modulates STIM1-dependent calcium entry Invited Reviewed International journal

    Yoko Fujii, Masayuki Shiota, Yasuyuki Ohkawa, Akemi Baba, Hideki Wanibuchi, Tatsuo Kinashi, Tomohiro Kurosaki, Yoshihiro Baba

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS   422 ( 4 )   615 - 620   2012.6

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1016/j.bbrc.2012.05.037

  • Impact of Ca2+ signaling on B cell function Reviewed

    Yoshihiro Baba, Tomohiro Kurosaki

    Trends in Immunology   32 ( 12 )   589 - 594   2011.12

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1016/j.it.2011.09.004

  • The Calcium Sensors STIM1 and STIM2 Control B Cell Regulatory Function through Interleukin-10 Production Reviewed

    Masanori Matsumoto, Yoko Fujii, Akemi Baba, Masaki Hikida, Tomohiro Kurosaki, Yoshihiro Baba

    Immunity   34 ( 5 )   703 - 714   2011.5

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1016/j.immuni.2011.03.016

  • Ca2+ signaling and STIM1 Invited Reviewed International journal

    Kurosaki T, Yoshihiro Baba

    PROGRESS IN BIOPHYSICS & MOLECULAR BIOLOGY   103 ( 1 )   51 - 58   2010.9

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1016/j.pbiomolbio.2010.02.004

  • S-glutathionylation activates STIM1 and alters mitochondrial homeostasis Invited Reviewed International journal

    Brian J Hawkinds, Krishna M Irrinki, Karthik Mallilankaraman, Yu-Chin Lien, Youjun Wang, Cunnigaiper D Bhanumathy, Ramasamy Subbiah, Michael F Ritchie, Jonathan Soboloff, Yoshihiro Baba, Tomohiro Kurosaki, Suresh K Joseph, Donald L Gill, Muniswamy Madesh.

    JOURNAL OF CELL BIOLOGY   190 ( 3 )   391 - 405   2010.8

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1083/jcb.201004152

  • B cell signaling and fate decision Reviewed

    Tomohiro Kurosaki, Hisaaki Shinohara, Yoshihiro Baba

    Annual Review of Immunology   28   21 - 55   2010.4

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1146/annurev.immunol.021908.132541

  • A novel stim1-dependent, non-capacitative Ca2+ entry pathway is activated by B cell receptor stimulation and depletion of Ca2+ stores Reviewed

    Takao Morita, Akihiko Tanimura, Yoshihiro Baba, Tomohiro Kurosaki, Yosuke Tojyo

    Journal of Medical Investigation   56 ( SUPPL. 1 )   383 - 387   2009.12

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.2152/jmi.56.383

  • Physiological function and molecular basis of STIM1-mediated calcium entry in immune cells Reviewed

    Yoshihiro Baba, Tomohiro Kurosaki

    Immunological Reviews   231 ( 1 )   174 - 188   2009.9

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1111/j.1600-065X.2009.00813.x

  • STIM protein coupling in the activation of Orai channels Reviewed

    Youjun Wang, Xiaoxiang Deng, Yandong Zhou, Eunan Hendron, Salvatore Mancarella, Michael F. Ritchie, Xiang D. Tang, Yoshihiro Baba, Tomohiro Kurosaki, Yasuo Mori, Jonathan Soboloff, Donald L. Gill

    Proceedings of the National Academy of Sciences of the United States of America   106 ( 18 )   7391 - 7396   2009.5

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1073/pnas.0900293106

  • A Stim1-dependent, noncapacitative Ca2+-entry pathway is activated by B-cell-receptor stimulation and depletion of Ca2+ Reviewed

    Takao Morita, Akihiro Tanimura, Yoshihiro Baba, Tomohiro Kurosaki, Yosuke Tojyo

    Journal of Cell Science   122 ( 8 )   1220 - 1228   2009.4

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1242/jcs.041640

  • Contrasting responses of lymphoid progenitors to canonical and noncanonical Wnt signals Reviewed

    Sachin Malhotra, Yoshihiro Baba, Karla P. Garrett, Frank J.T. Staal, Rachel Gerstein, Paul W. Kincade

    Journal of Immunology   181 ( 6 )   3955 - 3964   2008.9

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.4049/jimmunol.181.6.3955

  • Essential function for the calcium sensor STIM1 in mast cell activation and anaphylactic responses Invited Reviewed International journal

    Yoshihiro Baba, Keigo Nishida, Yoko Fujii, Toshio Hirano, Masaki Hikida, Tomohiro Kurosaki.

    NATURE IMMUNOLOGY   9 ( 1 )   81 - 88   2008.1

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1038/ni1546

  • Regulation of store-operated calcium entry by STIM1 Reviewed

    Yoshihiro Baba, Tomohiro Kurosaki

    Seikagaku   80 ( 12 )   1123 - 1128   2008

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    Language：English   Publishing type：Research paper (scientific journal)  

  • Coupling of STIM1 to store-operated Ca2+ entry through its constitutive and inducible movement in the endoplasmic reticulum Invited Reviewed International journal

    Yoshihiro Baba, Kenji Hayashi, Yoko Fujii, Akiko Mizushima, Hiroshi Watarai, Minoru Wakamori, Takuro Numaga, Yasuo Mori, Masamitsu Iino, Masaki Hikida, Tomohiro Kurosaki.

    PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA   103 ( 45 )   16704 - 16709   2006.11

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1073/pnas.0608358103

  • Constitutively active β-catenin promotes expansion of multipotent hematopoietic progenitors in culture Reviewed

    177 ( 4 )   2294 - 2303   2006.8

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    This study was designed to investigate one component of the Wnt/β-catenin signaling pathway that has been implicated in stem cell self-renewal. Retroviral-mediated introduction of stable β-catenin to primitive murine bone marrow cells allowed the expansion of multipotential c-KitlowSca-1low/-CD19- CD11b/Mac-1 -Flk-2-CD43+AA4.1 +NK1.1+CD3-CD11c-Gr-1 -CD45R/B220+ cells in the presence of stromal cells and cytokines. They generated myeloid, T, and B lineage lymphoid cells in culture, but had no T lymphopoietic potential when transplanted. Stem cell factor and IL-6 were found to be minimal requirements for long-term, stromal-free propagation, and a β-catenin-transduced cell line was maintained for 5 mo with these denned conditions. Although multipotential and responsive to many normal stimuli in culture, it was unable to engraft several types of irradiated recipients. These findings support previous studies that have implicated the canonical Wnt pathway signaling in regulation of multipotent progenitors. In addition, we demonstrate how it may be experimentally manipulated to generate valuable cell lines.

  • NF-κB is dispensable for normal lymphocyte development in bone marrow but required for protection of progenitors from TNFα Reviewed

    18 ( 5 )   653 - 659   2006.5

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    Language：English   Publishing type：Research paper (scientific journal)  

    Levels of the nuclear factor-kappa B (NF-κB)/Rel family of proteins are carefully modulated in differentiating lymphocytes, where these transcription factors are thought to be important for survival and fate decisions. In contrast, gene-targeting experiments have not revealed clear roles for these transcription factors in lymphopoiesis within bone marrow. Inhibition of NF-κB by introduction of mutated IκBα, a 'superinhibitor' of NF-κB, into hematopoietic stem cells or early progenitors suppressed B as well as T lymphopoiesis following transplantation into immunodeficient mice. Furthermore, a NF-κB essential modifier-binding domain (NBD) peptide that blocks IKB kinase (IKK) activity selectively impaired the generation of adult B lineage cells. However, this suppression did not occur when a neutralizing antibody to tumor necrosis factor α (TNFα) was added to the cultures, or in circumstances where few non-lymphoid cells were present. We conclude that while NF-κB plays a survival-promoting role in lymphoid progenitors, this may only be significant in circumstances such as transplantation when levels of TNFα are high.

    DOI： 10.1093/intimm/dxl002

  • Constitutively active beta-catenin confers multilineage differentiation potential on lymphoid and myeloid progenitors Invited Reviewed International journal

    Yoshihiro Baba, Karla P Garrett, Paul W Kincade.

    IMMUNITY   23 ( 6 )   599 - 609   2005.12

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1016/j.immuni.2005.10.009

  • IL-6 blocks a discrete early step in lymphopoiesis Invited Reviewed International journal

    Kazuhiko Maeda, Yoshihiro Baba, Yoshinori Nagai, Kozo Miyazaki, Alexander Malykhin, Koji Nakamura, Paul W Kincad, Nobuo Sakaguchi, K Mark Coggeshall.

    BLOOD   106 ( 3 )   879 - 885   2005.8

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1182/blood-2005-02-0456

  • Lymphoid progenitors and primary routes to becoming cells of the immune system Invited Reviewed International journal

    Rosana Pelayo, Rob Welner, S Scott Perry, Jiaxue Huang, Yoshihiro Baba, Takafumi Yokota, Paul W Kincade

    CURRENT OPINION IN IMMUNOLOGY   17 ( 2 )   100 - 107   2005.4

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1016/j.coi.2005.01.012

  • Relationships between hematopoietic stem cells and lymphocyte progenitors Invited Reviewed International journal

    Yoshihiro Baba, Rosana Pelayo, Paul W Kincade.

    TRENDS IN IMMUNOLOGY   25 ( 12 )   645 - 649   2004.12

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1016/j.it.2004.09.010

  • Preferential expression of the vasoactive intestinal peptide (VIP) receptor VPAC1 in human cord blood-derived CD34(+)CD38(-) cells: possible role of VIP as a growth-promoting factor for hematopoietic stem/progenitor cells Invited Reviewed International journal

    M. Kawakami, T. Kimura, Y. Kishimoto, T. Tatekawa, Y. Baba, T. Nishizaki, N. Matsuzaki, Y. Taniguchi, S. Yoshihara, K. Ikegame, T. Shirakata, S. Nishida, T. Masada, N. Hosen, A. Tsuboi, Y Oji, Y. Oka, H. Ogawa, Y. Sonoda, H. Sugiyama, I. Kawase, T. Soma.

    LEUKEMIA   18 ( 5 )   912 - 921   2004.5

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1038/sj.leu.2403330

  • Four Tyrosine Residues in Phospholipase C-γ2, Identified as Btk-dependent Phosphorylation Sites, Are Required for B Cell Antigen Receptor-coupled Calcium Signaling Reviewed

    276 ( 42 )   38595 - 38601   2001.10

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    Activation of phospholipase C-γ2 (PLCγ2) is the critical step in B cell antigen receptor (BCR)-coupled calcium signaling. Although genetic dissection experiments on B cells have demonstrated that Bruton's tyrosine kinase (Btk) and Syk are required for activating PLCγ2, the exact activation mechanism of PLCγ2 by these kinases has not been established. We identify the tyrosine residues 753, 759, 1197 and 1217 in rat PLCγ2 as Btk-dependent phosphorylation sites by using an in vitro kinase assay. To evaluate the role of these tyrosine residues in phosphorylation-dependent activation of PLCγ2, PLCγ2-deficient DT40 cells were reconstituted with a series of mutant PLCγ2s in which the phenylalanine was substituted for tyrosine. Substitution of all four tyrosine residues almost completely eliminated the BCR-induced PLCγ2 phosphorylation, indicating that these residues include the major phosphorylation sites upon BCR engagement. Cells expressing PLCγ2 with a single substitution exhibited some extent of reduction in calcium mobilization, whereas those expressing quadruple mutant PLCγ2 showed greatly reduced calcium response. These findings indicate that the phosphorylations of the tyrosine residues 753, 759, 1197, and 1217, which have been identified as Btk-dependent phosphorylation sites in vitro, coordinately contribute to BCR-induced activation of PLCγ2.

    DOI： 10.1074/jbc.M103675200

  • Bruton's tyrosine kinase is present in normal platelets and its absence identifies patients with X-linked agammaglobulinaemia and carrier females Reviewed

    Takeshi Futatani, Chiaki Watanabe, Yoshihiro Baba, Satoshi Tsukada, Hans D. Ochs

    British Journal of Haematology   114 ( 1 )   141 - 149   2001.8

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1046/j.1365-2141.2001.02905.x

  • BLNK mediates Syk-dependent Btk activation Reviewed

    Yoshihiro Baba, Shoji Hashimoto, Masato Matsushita, Dai Watanabe, Tadamitsu Kishimoto, Tomohiro Kurosaki, Satoshi Tsukada

    Proceedings of the National Academy of Sciences of the United States of America   98 ( 5 )   2582 - 2586   2001.2

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1073/pnas.051626198

  • Btk and BLNK in B cell development Reviewed

    Satoshi Tsukada, Yoshihiro Baba, Dai Watanabe

    Advances in Immunology   77   123 - 162   2001.1

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1016/S0065-2776(01)77016-2

  • Assignment of SH3BP5/Sh3bp5 encoding Sab, an SH3 domain-binding protein which preferentially associates with Bruton's tyrosine kinase, to human chromosome 1q43 and mouse chromosome 14B by in situ hybridization Reviewed

    Yoshihiro Baba, M. Matsushita, Y. Matsuda, J. Inazawa, T. Yamadori, S. Hashimoto, T. Kishimoto, Satoshi Tsukada

    Cytogenetics and Cell Genetics   87 ( 3-4 )   221 - 222   1999.12

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  • Identification of the SH2 domain binding protein of Bruton's tyrosine kinase as BLNK - Functional significance of Btk-SH2 domain in B-cell antigen receptor-coupled calcium signaling Reviewed

    Shoji Hashimoto, Akihiro Iwamatsu, Masamichi Ishiai, Katsuya Okawa, Tomoki Yamadori, Masato Matsushita, Yoshihiro Baba, Tadamitsu Kishimoto, Tomohiro Kurosaki, Satoshi Tsukada

    Blood   94 ( 7 )   2357 - 2364   1999.10

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  • Bruton's tyrosine kinase activity is negatively regulated by Sab, the Btk-SH3 domain-binding protein Reviewed

    Tomoki Yamadori, Yoshihiro Baba, Masato Matsushita, Shoji Hashimoto, Mari Kurosaki, Tomohiro Kurosaki, Tadamitsu Kishimoto, Satoshi Tsukada

    Proceedings of the National Academy of Sciences of the United States of America   96 ( 11 )   6341 - 6346   1999.5

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1073/pnas.96.11.6341

  • Involvement of Wiskott-Aldrich syndrome protein in B-cell cytoplasmic tyrosine kinase pathway Reviewed

    Yoshihiro Baba, Shigeaki Nonoyama, Masato Matsushita, Tomoki Yamadori, Shoji Hashimoto, Kohsuke Imai, Shigeyuki Arai, Toshio Kunikata, Masashi Kurimoto, Tomohiro Kurosaki, Hans D. Ochs, Jun Ichi Yata, Tadamitsu Kishimoto, Satoshi Tsukada

    Blood   93 ( 6 )   2003 - 2012   1999.3

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  • Bruton's Tyrosine Kinase (BTK) is present in normal platelets, and its absence identifies patients with X-Linked Agammaglobulinemia (XLA) and carrier females Reviewed

    C. Watanabe, T. Futatani, Yoshihiro Baba, S. Tsukada, A. Oda, H. D. Ochs

    Journal of Investigative Medicine   47 ( 2 )   1999

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  • Identification and characterization of a novel SH3-domain binding protein, Sab, which preferentially associates with Bruton's tyrosine kinase (Btk) Reviewed

    Masato Matsushita, Tomoki Yamadori, Seishi Kato, Yoshihiro Takemoto, Jouji Inazawa, Yoshihiro Baba, Shoji Hashimoto, Shingo Sekine, Shigeyuki Arai, Toshio Kunikata, Masashi Kurimoto, Tadamitsu Kishimoto, Satoshi Tsukada

    Biochemical and Biophysical Research Communications   245 ( 2 )   337 - 343   1998.4

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1006/bbrc.1998.8420

  • Involvement of Wiskott-Aldrich Syndrome Protein (WASP) in B cell antigen receptor and Btk signaling pathway Reviewed

    Yoshihiro Baba, S. Nonoyama, K. Imai, H. D. Ochs, J. Yata, T. Kishimoto

    FASEB Journal   12 ( 5 )   1998.3

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  • The 21-kDa polypeptide (VAP21) in the rabies virion is a CD99-related host cell protein Reviewed

    Junji Sagara, Tadafumi S. Tochikura, Hajime Tanaka, Yoshihiro Baba, Shoichiro Tsukita, Sachiko Tsukita, Akihiko Kawai

    MICROBIOLOGY and IMMUNOLOGY   42 ( 4 )   289 - 297   1998.1

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    Language：English   Publishing type：Research paper (scientific journal)  

    DOI： 10.1111/j.1348-0421.1998.tb02285.x

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    丸善出版  2023    （ ISBN:9784621308011 ）

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    Language：Japanese  

    CiNii Books

  • 腎臓内科

    今林慶祐、馬場義裕

    2022.6 

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    Language：Japanese  

  • 標準免疫学

    馬場義裕（ Role： Joint author）

    医学書院  2021.3 

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    Responsible for pages：P185-193   Language：Japanese   Book type：Scholarly book

Presentations

  • 自己免疫疾患における病原性B細胞

    馬場義裕

    第15回日本血液疾患免疫療法学会,  2023.6 

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    Event date： 2023.6

    Language：Japanese  

    Country：Japan  

  • 静止期のB細胞は、B細胞受容体シグナルにより抗がん剤感受性となる

    #細川尊夏、@田中伸弥、@森健、@馬場義裕、@片山佳樹

    第38回 日本DDS学会学術集会  2022.6 

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    Event date： 2023.6

    Language：Japanese  

    Country：Japan  

  • B細胞による免疫応答制御と疾患病態への関与

    馬場 義裕

    第10回神経と免疫を語る会  2022.7 

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    Event date： 2023.6

    Language：Japanese  

    Country：Japan  

  • B細胞の免疫応答制御

    馬場義裕

    第23回日本免疫学会サマースクール  2022.8 

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    Event date： 2023.6

    Language：Japanese  

    Country：Japan  

  • B cell dysfunction in self-tolerance and autoimmune disease

    The 31st Hot Spring Harbor International Symposium  2022.11 

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    Event date： 2023.6

    Language：Japanese  

    Country：Japan  

  • Variant histone H3.3 expression controls the plasma cell differentiation．

    13. 齋藤雄一，原田哲二，大川恭行，馬場義裕

    第51回日本免疫学会学術集会  2022.12 

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    Event date： 2023.6

    Language：Japanese  

    Country：Japan  

  • Essential function for EMC1(ER membrane complex subunit1) in Ca2+ influx and B cell development

    Kazuhiko Kawata, Chie Kikutake, Mikita Suyama, Yoshihiro Baba

    2022.12 

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    Event date： 2023.6

    Language：Japanese  

    Country：Japan  

  • STIM-mediated store-operated calcium entry regulates maintenance and selection of germinal center B cells

    11. Yutaro Yada, Masanori Matsumoto, Takeshi Inoue, Daisuke Kitamura, Tomohiro Kurosaki and Yoshihiro Baba

    2022.12 

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    Event date： 2023.6

    Language：Japanese  

    Country：Japan  

  • The role of Fcrl5 in autoimmune disease

    Chisato Ono, Yuta Kochi, Shinya Tanaka, Kazuhiko Yamamoto, Yoshihiro Baba

    2022.12 

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    Event date： 2023.6

    Language：Japanese  

    Country：Japan  

  • The Bruton’s tyrosine kinase (Btk) inhibitor acalabrutinib suppress LPS-induced sepsis via inhibition of marginal zone B cells activation.

    第51回日本免疫学会学術集会  2022.12 

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    Event date： 2023.6

    Language：Japanese  

    Country：Japan  

  • Essential role of ER membrane complex subunit 1 (EMC1) in B cell development.

    #Kazuhiko Kawata, @Yoshihiro Baba.

    2023.6 

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    Event date： 2023.6

    Language：Japanese  

    Country：Japan  

  • B細胞を起点とする免疫応答制御と疾患病態

    馬場義裕

    2023.6 

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    Event date： 2023.6 - 2023.3

    Language：Japanese  

    Country：Japan  

  • B細胞の免疫応答制御 Invited

    馬場義裕

    令和3年第四回東名産学官・医連携研究会  2022.2 

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    Event date： 2022.2

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：web開催   Country：Japan  

  • 免疫アレルギー疾患を正負に制御するB細胞 Invited

    馬場義裕

    第70回日本アレルギー学会学術大会  2021.10 

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    Event date： 2021.10

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：web開催   Country：Japan  

  • B細胞の免疫応答制御 Invited

    馬場義裕

    第22回日本免疫学会サマースクール  2021.9 

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    Event date： 2021.9

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：web開催   Country：Japan  

  • B細胞による自己免疫疾患制御 Invited

    馬場義裕

    免疫と神経疾患オンラインセミナー  2020.12 

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    Event date： 2020.12

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：web開催   Country：Japan  

  • B細胞の免疫応答制御機構 Invited

    馬場義裕

    第16回皮膚免疫疾患研究会  2020.10 

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    Event date： 2020.10

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：web開催   Country：Japan  

  • B細胞の免疫応答制御機構 Invited

    馬場義裕

    がん免疫セミナー（千葉）  2019.6 

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    Event date： 2019.6

    Language：Japanese   Presentation type：Public lecture, seminar, tutorial, course, or other speech  

    Venue：千葉   Country：Japan  

  • B細胞の免疫応答制御機構 Invited

    馬場義裕

    がん免疫セミナー（東京）  2019.6 

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    Event date： 2019.6

    Language：Japanese   Presentation type：Public lecture, seminar, tutorial, course, or other speech  

    Venue：東京   Country：Japan  

  • B細胞はどのようにして免疫応答を制御するのか Invited

    馬場義裕

    第93回染色体工学研究センターセミナー  2019.6 

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    Event date： 2019.6

    Language：Japanese   Presentation type：Public lecture, seminar, tutorial, course, or other speech  

    Venue：鳥取県米子市   Country：Japan  

  • アレルギー発症と制御におけるB細胞の役割 Invited

    馬場義裕

    日本アレルギー学会第5回総合アレルギー講習会  2018.12 

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    Event date： 2018.12

    Language：Japanese   Presentation type：Oral presentation (general)  

    Country：Japan  

  • Humoral immunity and diseases Invited

    2018.11 

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    Event date： 2018.12

    Language：Japanese   Presentation type：Oral presentation (general)  

    Country：Japan  

  • B細胞による炎症制御機構 Invited

    馬場義裕

    第9回中国免疫不全症研究会  2018.7 

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    Event date： 2018.7

    Language：Japanese   Presentation type：Oral presentation (general)  

    Country：Japan  

  • 炎症を制御するIL-10産生B細胞の誘導機序 Invited

    馬場 義裕

    第43回日本臨床免疫学総会  2017.10 

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    Event date： 2017.10

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：神戸   Country：Japan  

  • 胚中心B細胞におけるカルシウム流入の役割 Invited

    馬場 義裕

    生体機能と創薬シンポジウム 2017  2017.8 

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    Event date： 2017.8

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：京都   Country：Japan  

  • B細胞による炎症制御機構 Invited

    馬場 義裕

    第8回 Q-PID 九州地区免疫不全症研究会  2017.7 

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    Event date： 2017.7

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：福岡   Country：Japan  

  • Regulatory function of B cells in autoimmune inflammation Invited International conference

    Yoshihiro Baba

    The 7th IFReC International Symposium "Immunology at the Forefront"  2016.1 

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    Event date： 2016.1

    Language：English   Presentation type：Symposium, workshop panel (public)  

    Country：Japan  

  • B細胞ストア作動性カルシウム流入による自己免疫性炎症反応の制御機構 Invited

    馬場 義裕

    日本薬学会第135回年会  2015.3 

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    Event date： 2015.3

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：神戸学院大学、神戸   Country：Japan  

  • The mechanism of calcium influx induced by ER calcium sensor STIM and its physiological function Invited

    2012.12 

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    Event date： 2012.12

    Language：Japanese   Presentation type：Oral presentation (general)  

    Country：Japan  

  • Physiological significance for Calcium Influx in B cell Invited

    2012.9 

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    Event date： 2012.9

    Language：Japanese   Presentation type：Oral presentation (general)  

    Country：Japan  

  • B細胞におけるカルシウム流入の生理的役割 Invited

    馬場 義裕, 松本 真典, 黒崎 知博

    第132回 日本薬学会年会  2012.3 

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    Event date： 2012.3

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：札幌   Country：Japan  

  • Essential role of Ca2+ influx in B cell regulatory function Invited International conference

    Yoshihiro Baba

    2011.12 

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    Event date： 2011.12

    Language：English   Presentation type：Oral presentation (general)  

    Country：Japan  

  • Store-Operated Calcium Entry in Regulatory Function of B cell Invited

    2011.7 

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    Event date： 2011.7

    Language：Japanese   Presentation type：Oral presentation (general)  

    Country：Japan  

  • Store-Operated Calcium Entry in Regulatory Function of B cell Invited

    2010.7 

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    Event date： 2010.7

    Language：Japanese   Presentation type：Oral presentation (general)  

    Country：Japan  

  • B細胞における小胞体カルシウムセンサーSTIMの生理的役割 Invited

    馬場 義裕, 松本 真典, 黒崎 知博

    第83回日本薬理学会年会シンポジウム  2010.3 

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    Event date： 2010.3

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：大阪国際会議場, 大阪   Country：Japan  

  • Store-operated Calcium Entry in B cells Invited

    2009.12 

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    Event date： 2009.12

    Language：Japanese   Presentation type：Oral presentation (general)  

    Country：Japan  

  • Essential role of STIM1, ER calcium sensor, for store-operated calcium influx and mast cell activation Invited

    2009.9 

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    Event date： 2009.9

    Language：Japanese   Presentation type：Oral presentation (general)  

    Country：Japan  

  • ストア作動性カルシウムチャネル複合体の形成機構とその生理的役割 Invited

    馬場 義裕

    特定領域研究「膜輸送複合体」班会議  2009.8 

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    Event date： 2009.8

    Language：Japanese   Presentation type：Oral presentation (general)  

    Country：Japan  

  • Physiological function for store-operated calcium entry in immune response Invited International conference

    Yoshihiro Baba

    2009.2 

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    Event date： 2009.2

    Language：English   Presentation type：Oral presentation (general)  

    Country：Japan  

  • ストア作動性カルシウムチャネル複合体の形成機構とその生理的役割 Invited

    馬場 義裕

    Gタンパク質特定領域・膜輸送複合体特定領域 合同若手ワークショップ 2009  2009.1 

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    Event date： 2009.1

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：神戸セミナーハウス, 兵庫   Country：Japan  

  • Essential role of STIM1, ER calcium sensor, for store-operated calcium influx and mast cell activation Invited

    2008.6 

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    Event date： 2008.6

    Language：Japanese   Presentation type：Oral presentation (general)  

    Country：Japan  

  • STIM1によるストア作動性カルシウム流入メカニズム Invited

    馬場 義裕

    第８回硬組織研究セミナー  2008.5 

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    Event date： 2008.5

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：慶応大学医学部, 東京   Country：Japan  

  • マスト細胞活性化におけるSTIM1の役割 Invited

    馬場 義裕

    第１７回東京免疫フォーラム  2008.3 

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    Event date： 2008.3

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：東京大学医科学研究所, 東京   Country：Japan  

  • Essential role for STIM1 in mast cell activation and anaphylactic responses Invited

    2007.10 

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    Event date： 2007.10

    Language：Japanese   Presentation type：Oral presentation (general)  

    Country：Japan  

  • STIM1を介したB細胞抗原受容体刺激によるストア作動性カルシウム流入誘発機構 Invited

    馬場 義裕, 黒崎 知博

    平成18年度 生理学研究所研究会  2006.10 

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    Event date： 2006.10

    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：岡崎コンファレンスセンター, 愛知   Country：Japan  

  • Constitutive Signaling via the Wnt/b-catenin Pathway Disrupts Differentiation and Confers Multi-lineage Differentiation on Lympho-Myeloid Progenitors Invited International conference

    Yoshihiro Baba, Yokota T., Kincade PW.

    2005.4 

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    Language：English   Presentation type：Oral presentation (general)  

    Country：Japan  

  • Development of IL-17A+ Vγ6 γδ T cells in mouse thymus

    第48回日本免疫学会  2019.12 

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    Language：Japanese  

    Country：Japan  

  • Ten-eleven translocaion (Tet) in B cells prevent autoimmunity.

    Tanaka S, Ise W, Kurosaki T, Baba Y.

    2019.12 

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    Language：Japanese  

    Country：Japan  

  • Role of Fcrl5 in B cell immune response and peripheral tolerance.

    #Ono C, #Kochi Y, Tanaka S, Yamamoto K, Baba Y.

    2019.12 

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    Language：Japanese  

    Country：Japan  

  • 免疫反応を抑制するB細胞 Invited

    馬場義裕

    第18回レジェンドセミナー  2019.12 

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    Language：Japanese   Presentation type：Oral presentation (general)  

    Venue：浜松   Country：Japan  

  • 自然免疫(2) Innate recognitionおよびシグナル伝達　ブルトン型チロシンキナーゼ(Btk)阻害剤acalabrutinibは辺縁帯B細胞の活性化抑制を介してLPS誘発性敗血症を抑制する(Innate immunity(2) Innate recognition and signaling　The Bruton's tyrosine kinase(Btk) inhibitor acalabrutinib suppress LPS-induced sepsis via inhibition of marginal zone B cells activation)

    Hatano Shinya, Kawata Kazuhiko, Baba Yoshihiro

    日本免疫学会総会・学術集会記録  2022.11  (NPO)日本免疫学会

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    Language：English  

  • 形質細胞の分化はヒストン変異体H3.3の発現によって制御される(Plasma cell differentiation is regulated by the expression of histone variant H3.3)

    Saito Yuichi, Murakami Daisuke, Baba Yoshihiro, Harada Akihito, Ohkawa Yasuyuki, Takashi Nakagawa

    日本耳鼻咽喉科頭頸部外科学会会報  2024.4  (一社)日本耳鼻咽喉科頭頸部外科学会

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  • 免疫学的寛容と免疫抑制-2　自己免疫疾患におけるFcrl5の役割(Tolerance and Immune suppression-2　The role of Fcrl5 in autoimmune disease)

    Ono Chisato, Kochi Yuta, Tanaka Shinya, Yamamoto Kazuhiko, Baba Yoshihiro

    日本免疫学会総会・学術集会記録  2022.11  (NPO)日本免疫学会

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    Language：English  

  • マスサイトメトリー調査によるがん治療における肺炎の免疫表現型の解明(Unveiling the Immunophenotypes of Pneumonitis in Cancer Treatment Through Mass Cytometry Exploration)

    Yanagihara Toyoshi, Hata Kentaro, Matsubara Keisuke, Kunimura Kazufumi, Suzuki Kunihiro, Tsubouchi Kazuya, Ikegame Satoshi, Baba Yoshihiro, Fukui Yoshinori, Okamoto Isamu

    日本呼吸器学会誌  2024.3  (一社)日本呼吸器学会

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    Language：English  

  • I型インターフェロンがTLR9刺激濾胞B細胞の形質細胞分化の運命を決定する(Type I interferon determines the fate of TLR9-stimulated follicular B cells to plasma cell differentiation)

    Higuchi Ryota, Tanaka Kaori, Ohkawa Yasuyuki, Baba Yoshihiro

    日本免疫学会総会・学術集会記録  2023.12  (NPO)日本免疫学会

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    Language：English  

  • B細胞発生と活性化　EMC1(ER膜複合体サブユニット1)のCa2+流入とB細胞発生における必須機能(B cell Development and Activation　Essential function for EMC1(ER membrane complex subunit1) in Ca2+ influx and B cell development)

    Kawata Kazuhiko, Kikutake Chie, Suyama Mikita, Baba Yoshihiro

    日本免疫学会総会・学術集会記録  2022.11  (NPO)日本免疫学会

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    Language：English  

  • B細胞におけるケモカイン受容体のCa2+流入と生合成におけるEMC1(ER membrane complex subunit1)の本質的な機能(Essential function of EMC1(ER membrane complex subunit1) in Ca2+ influx and biogenesis of chemokine receptors in B cell)

    Kawata Kazuhiko, Kikutake Chie, Suyama Mikita, Baba Yoshihiro

    日本免疫学会総会・学術集会記録  2023.12  (NPO)日本免疫学会

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    Language：English  

  • B細胞(1)　誕生から死まで　慢性的なBCRシグナル伝達がアネルギー性B細胞からage-associated B細胞の生成と維持を形作る(B cell: from birth to death　Chronic BCR signaling shapes the generation and maintenance of age-associated B cells from anergic B cells)

    Imabayashi Keisuke, Niiro Hiroaki, Baba Yoshihiro

    日本免疫学会総会・学術集会記録  2023.12  (NPO)日本免疫学会

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    Language：English  

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MISC

  • 【ヒト疾患と免疫細胞サブセット　解像度をあげて見えてきた病態を規定する疾患のキープレーヤーと治療戦略】(第2章)獲得免疫系　免疫応答を正負に制御するB細胞サブセット

    今林 慶祐, 馬場 義裕

    実験医学   42 ( 12 )   1889 - 1896   2024.8   （ ISSN:0288-5514 ）

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    Language：Japanese   Publisher：(株)羊土社  

    B細胞は抗体産生,免疫記憶,サイトカインの分泌を介して生体防御免疫を担うが,機能によるB細胞サブセットの多様性が自己免疫疾患との関連において注目されている.自己免疫反応を抑制するB細胞のサブセットとしてregulatory B cells(制御性B細胞)が同定され,一方,自己免疫反応を促進するB細胞のサブセットとしてage-associated B cells(加齢性B細胞,ABCs)が同定され,脚光を浴びている.これらのB細胞の分化や維持のメカニズム,そして疾患への関与を理解することは,自己免疫疾患の病態の理解や治療開発に必須である.本稿では,免疫応答を正負に制御するB細胞サブセットについて概説する.(著者抄録)

  • 胚中心B細胞のポジティブセレクションにおけるカルシウムシグナル

    矢田 裕太郎, 馬場 義裕

    臨床免疫・アレルギー科   81 ( 5 )   491 - 496   2024.5   （ ISSN:1881-1930 ）

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    Language：Japanese   Publisher：(有)科学評論社  

  • いま知りたい!!　免疫のブレーキ"制御性B細胞"研究から疾患制御へ

    川上 亮, 馬場 義裕

    実験医学   41 ( 13 )   2140 - 2146   2023.8   （ ISSN:0288-5514 ）

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    Language：Japanese   Publisher：(株)羊土社  

    B細胞は抗体産生,免疫記憶,サイトカイン産生を介して生体防御免疫を促進するが,自己免疫疾患においては増悪因子として機能する.一方で,B細胞のうち制御性B細胞とよばれるサブセットが,IL-10などの抗炎症性サイトカインの分泌や細胞表面抑制性分子による細胞間相互作用によって多種多様な免疫応答を制御することは20年以上前から報告され,その重要性が指摘されている.しかし,制御性B細胞が疾患環境や作用機序の違いにより多様な顔を見せることから,包括的な理解は今後の課題である.本稿では,制御性B細胞の重要性ならびに,研究や医療応用に向けた知見について紹介する.(著者抄録)

  • 老化と免疫

    今林 慶祐, 馬場 義裕

    腎臓内科   16 ( 4 )   483 - 489   2022.10   （ ISSN:2435-1903 ）

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    Language：Japanese   Publisher：(有)科学評論社  

  • アレルギー発症と制御におけるB細胞の役割

    齋藤雄一、馬場義裕

    アレルギー   2019.6

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    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • 制御性B細胞と疾患

    川上亮、馬場義裕

    炎症と免疫（先端医学社）   2018.9

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    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • 「抗体の多様性」「抗体のクラススイッチ」「B細胞抗原受容体」「抗原ー抗体反応と免疫複合体」

    馬場 義裕

    免疫ペディア（羊土社）   2017.6

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    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • B細胞ストア作動性カルシウム流入による自己免疫性炎症反応の制御機構

    馬場 義裕

    YAKUGAKU ZASSHI 薬学雑誌   2016.3

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    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • 免疫反応を抑制するB細胞：制御性B細胞

    馬場 義裕

    ライフサイエンス領域融合レビュー   2016.1

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    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • B細胞による腫瘍制御

    馬場 義裕

    The Frontiers in Life Sciences　がんと免疫（南山堂）   2015.10

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    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • IL-10産生B細胞による自己免疫疾患の制御

    馬場 義裕, 黒崎 知博

    実験医学増刊号　自己免疫疾患 （羊土社）   2015.7

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    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • インターロイキン10を産生するプラズマブラストは自己免疫疾患における炎症反応を抑制する

    松本 真典, 黒崎 知博, 馬場 義裕

    ライフサイエンス 新着論文レビュー   2014.12

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    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • B細胞からのIL-10産生機序

    馬場 義裕

    臨床免疫・アレルギー科（科学評論社）   2013.9

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    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • 制御性B 細胞におけるSTIM依存的カルシウム流入の役割

    松本 真典, 馬場 義裕

    YAKUGAKU ZASSHI　薬学雑誌   2013.4

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    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • B細胞のCa2+シグナルと自己免疫性炎症反応の抑制

    馬場 義裕, 黒崎 知博

    医学のあゆみ（医歯薬出版社）   2012.1

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    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • ストア作動性カルシウムチャネル

    馬場 義裕

    細胞（ニューサイエンス社）   2011.10

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    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • 免疫細胞におけるストア作動性カルシウム流入の役割

    馬場 義裕

    日本薬理学雑誌   2011.5

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    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • 小胞体Ca2+センサーであるSTIM1とSTIM2の誘導するCa2+流入がB細胞のインターロイキン10産生および炎症抑制機能に必須である

    馬場 義裕

    ライフサイエンス 新着論文レビュー   2011.5

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    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • トランスポートソームの世界：免疫系

    馬場 義裕

    京都廣川書店   2011.3

    　More details

    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • STIM1によるカルシウム応答の制御機構

    馬場 義裕, 黒崎 知博

    生化学   2008.12

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    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • マストセルの小胞体カルシウムセンサー

    馬場 義裕, 黒崎 知博

    感染・炎症・免疫   2008.12

    　More details

    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • Ca2+シグナルとSTIM1

    馬場 義裕, 黒崎 知博

    実験医学増刊シグナル伝達研究2008-2009（羊土社）   2008.9

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    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • 小胞体Ca2+センサーSTIM1が誘導するCa2+流入がマスト細胞活性化に必須である

    馬場 義裕

    実験医学   2008.4

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    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • Tecファミリーキナーゼ

    馬場 義裕, 塚田 聡

    新用語ライブラリー免疫（羊土社）   1999.10

    　More details

    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • 無ガンマグロブリン血症とBtk

    馬場 義裕, 塚田 聡

    遺伝子医学（メディカルドウ）   1999.8

    　More details

    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • BtkとWASP-２つの免疫不全症責任遺伝子の連関

    塚田 聡, 馬場 義裕

    免疫1998-99（中山書店）   1998.1

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    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • Btk

    1997.12

    　More details

    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • BtkとＢ細胞分化

    馬場 義裕, 塚田 聡

    医学のあゆみ（医歯薬出版社）   1997.4

    　More details

    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • 最近わかった先天性免疫不全症の責任遺伝子

    馬場 義裕, 塚田 聡

    感染・炎症・免疫 （医薬の門社）   1997.1

    　More details

    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • 先天性免疫グロブリン異常症

    馬場 義裕, 塚田 聡

    Molecular Medicine : 分子医学を臨床へ（中山書店）   1997.1

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    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

  • Ｂ細胞分化と免疫不全症

    馬場 義裕, 塚田 聡

    細胞工学（秀潤社）   1996.12

    　More details

    Language：Japanese   Publishing type：Article, review, commentary, editorial, etc. (scientific journal)  

▼display all

Industrial property rights

Patent   Number of applications: 1   Number of registrations: 0
Utility model   Number of applications: 0   Number of registrations: 0
Design   Number of applications: 0   Number of registrations: 0
Trademark   Number of applications: 0   Number of registrations: 0

Professional Memberships

  • Japanese Society for Immunology

Committee Memberships

  • 免疫学会   教育推進委員長   Domestic

    2021.4 - 2023.3   

  • 日本免疫学会   教育推進委員   Domestic

    2018.12 - 2023.12   

  • Councilor   Domestic

    2016.1 - 2020.12   

Academic Activities

  • Screening of academic papers

    Role(s)： Peer review

    2022

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    Type：Peer review 

    Number of peer-reviewed articles in foreign language journals：5

  • Screening of academic papers

    Role(s)： Peer review

    2021

    　More details

    Type：Peer review 

    Number of peer-reviewed articles in foreign language journals：8

  • Screening of academic papers

    Role(s)： Peer review

    2019

    　More details

    Type：Peer review 

    Number of peer-reviewed articles in foreign language journals：5

  • 座長

    日本免疫学会  （ 福岡 ） 2018.12 - 2019.6

    　More details

    Type：Competition, symposium, etc. 

  • 座長 International contribution

    日本小児感染症学会  （ 福岡 ） 2018.11 - 2019.6

    　More details

    Type：Competition, symposium, etc. 

  • Screening of academic papers

    Role(s)： Peer review

    2018

    　More details

    Type：Peer review 

    Number of peer-reviewed articles in foreign language journals：10

  • 座長（Chairmanship）

    第42回日本免疫学会  2013.12 - Present

    　More details

    Type：Competition, symposium, etc. 

  • 座長（Chairmanship） International contribution

    2012.1 - Present

    　More details

    Type：Competition, symposium, etc. 

  • 座長（Chairmanship） International contribution

    The 4th International Conference on “B Cells and Autoimmunity”  2010.8 - Present

    　More details

    Type：Competition, symposium, etc. 

  • シンポジウムオーガナイザー

    第87回日本生理学会大会シンポジウム  （ 盛岡市民文化ホール, 宮城 ） 2010.5

    　More details

    Type：Competition, symposium, etc. 

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Research Projects

  • Molecular basis of induction and activation of tissue-accumulated B cells and their pathological significance.

    Grant number：24K02297  2024.4 - 2027.3

    Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (B)

    　 More details

    Grant type：Scientific research funding

    CiNii Research

  • 病原性記憶B細胞による自己免疫応答メカニズムと疾患病態の理解

    2023.10 - 2029.3

    日本 

    　 More details

    Authorship：Principal investigator 

  • 病原性記憶B細胞による自己免疫応答メカニズムと疾患病態の理解

    2023 - 2027

    AMED CREST 革新的先端研究開発支援事業

    　 More details

    Authorship：Principal investigator  Grant type：Contract research

  • Understanding of the function of regulatory and pathogenic IgG4

    Grant number：21K18256  2021 - 2024

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Challenging Research(Pioneering)

    　 More details

    Authorship：Principal investigator  Grant type：Scientific research funding

    CiNii Research

  • 加齢に伴い変動するB細胞サブタイプの病態生理学的役割

    Grant number：21H02753  2021 - 2023

    日本学術振興会  科学研究費助成事業  基盤研究(B)

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    Authorship：Principal investigator  Grant type：Scientific research funding

  • 新規ヒト型IgG4産生マウスを用いたIgG4の病理的意義の解明

    Grant number：19K22537  2019 - 2020

    日本学術振興会  科学研究費助成事業  挑戦的研究（萌芽）

    　 More details

    Authorship：Principal investigator  Grant type：Scientific research funding

  • I型インターフェロンが誘導するB細胞機能の二面性と自己免疫疾患病態の理解

    Grant number：18H02626  2018 - 2020

    日本学術振興会  科学研究費助成事業  基盤研究(B)

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    Authorship：Principal investigator  Grant type：Scientific research funding

  • 液性免疫機能の経年劣化メカニズムの解明

    2017.10 - 2021.3

    国立研究開発法人日本医療研究開発機構 

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    Authorship：Principal investigator 

  • B細胞の免疫制御作用を起点とする自己免疫病態の理解とその応用

    2017.9 - 2020.3

    国立研究開発法人日本医療研究開発機構 

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    Authorship：Principal investigator 

  • 液性免疫機能の経年劣化メカニズムの解明

    2017 - 2020

    AMED 革新的先端研究開発支援事業

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    Authorship：Principal investigator  Grant type：Contract research

  • B細胞の免疫制御作用を起点とする自己免疫病態の理解とその応用

    2017 - 2019

    AMED　免疫アレルギー疾患等実用化研究事業

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    Authorship：Principal investigator  Grant type：Contract research

  • 新規ヒト制御性B細胞の選択的誘導法の開発

    Grant number：16K15217  2016 - 2018

    科学研究費助成事業  挑戦的萌芽研究

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    Authorship：Principal investigator  Grant type：Scientific research funding

  • B細胞による免疫抑制の分子機構と病理的意義

    Grant number：15H04746  2015 - 2017

    日本学術振興会  科学研究費助成事業  基盤研究(B)

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    Authorship：Principal investigator  Grant type：Scientific research funding

  • 制御性B細胞の実体と免疫抑制機序の解明

    Grant number：24689023  2012 - 2014

    科学研究費助成事業  若手研究(A)

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    Authorship：Principal investigator  Grant type：Scientific research funding

  • B細胞分化を規定する多階層遺伝子発現制御の同定

    Grant number：24659220  2012 - 2013

    科学研究費助成事業  挑戦的萌芽研究

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    Authorship：Principal investigator  Grant type：Scientific research funding

  • 制御性サイトカイン産生B細胞におけるカルシウム流入の生理的意義の解明

    Grant number：22021026  2010 - 2011

    科学研究費助成事業  特定領域研究

    　 More details

    Authorship：Principal investigator  Grant type：Scientific research funding

  • Ｂ細胞におけるストア作動性カルシウム流入の生理的役割とその分子基盤の解明

    Grant number：21790469  2009 - 2010

    科学研究費助成事業  若手研究(B)

    　 More details

    Authorship：Principal investigator  Grant type：Scientific research funding

  • ストア作動性カルシウムチャネル複合体の形成機構とその生理的役割

    Grant number：20056033  2008 - 2009

    科学研究費助成事業  特定領域研究

    　 More details

    Authorship：Principal investigator  Grant type：Scientific research funding

  • B細胞におけるSTIM1依存的カルシウム流入機構の解析

    Grant number：19790368  2007 - 2008

    科学研究費助成事業  若手研究(B)

    　 More details

    Authorship：Principal investigator  Grant type：Scientific research funding

▼display all

Class subject

  • 口腔免疫学

    2024.4 - 2024.9   First semester

  • 免疫学

    2024.4 - 2024.9   First semester

  • 口腔免疫学

    2023.10 - 2024.3   Second semester

  • 免疫学

    2023.4 - 2023.9   First semester

  • 免疫学

    2022.4 - 2022.9   First semester

  • 口腔免疫学

    2021.10 - 2022.3   Second semester

  • 免疫学

    2021.4 - 2021.9   First semester

  • 口腔免疫学

    2020.10 - 2021.3   Second semester

  • 免疫学

    2020.4 - 2020.9   First semester

  • 基礎医学

    2019.10 - 2020.3   Second semester

  • 免疫学

    2019.4 - 2019.9   First semester

  • 免疫学

    2018.4 - 2018.9   First semester

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Visiting, concurrent, or part-time lecturers at other universities, institutions, etc.

  • 2024  大阪大学免疫学フロンティア研究センター  Classification:Affiliate faculty  Domestic/International Classification:Japan 

  • 2024  山口東京理科大学  Classification:Affiliate faculty  Domestic/International Classification:Japan 

  • 2024  東京医科歯科大学  Classification:Affiliate faculty  Domestic/International Classification:Japan 

  • 2024  名古屋大学  Classification:Affiliate faculty  Domestic/International Classification:Japan 

  • 2023  東京医科歯科大学  Classification:Part-time lecturer  Domestic/International Classification:Japan 

  • 2023  名古屋大学  Classification:Affiliate faculty  Domestic/International Classification:Japan 

  • 2023  大阪大学免疫学フロンティア研究センター  Classification:Affiliate faculty  Domestic/International Classification:Japan 

  • 2022  大阪大学免疫学フロンティア研究センター  Classification:Affiliate faculty  Domestic/International Classification:Japan 

  • 2022  名古屋大学医学部  Classification:Part-time lecturer  Domestic/International Classification:Japan 

  • 2021  名古屋大学医学部  Classification:Part-time lecturer  Domestic/International Classification:Japan 

  • 2021  大阪大学免疫学フロンティア研究センター  Classification:Affiliate faculty  Domestic/International Classification:Japan 

  • 2020  大阪大学免疫学フロンティア研究センター  Classification:Affiliate faculty  Domestic/International Classification:Japan 

  • 2019  名古屋大学医学部  Classification:Part-time lecturer  Domestic/International Classification:Japan 

  • 2019  大阪大学免疫学フロンティア研究センター  Classification:Affiliate faculty  Domestic/International Classification:Japan 

  • 2018  大阪大学免疫学フロンティア研究センター  Classification:Affiliate faculty  Domestic/International Classification:Japan 

  • 2018  名古屋大学医学部  Classification:Part-time lecturer  Domestic/International Classification:Japan 

    Semester, Day Time or Duration：前期　6月

  • 2017  大阪大学免疫学フロンティア研究センター  Classification:Affiliate faculty  Domestic/International Classification:Japan 

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Outline of Social Contribution and International Cooperation activities

  • 学会運営,
    免疫サマースクール

Media Coverage

  • 多発性硬化症　悪化抑制 Newspaper, magazine

    読売新聞（夕刊3面）  2014.12

    　More details

    多発性硬化症　悪化抑制

  • 阪大、多発性硬化症抑える免疫細胞を確認−たんぱく質IL-10がB細胞集団から分泌 Newspaper, magazine

    日刊工業新聞  2014.12

    　More details

    阪大、多発性硬化症抑える免疫細胞を確認−たんぱく質IL-10がB細胞集団から分泌

  • 多発性硬化症　悪化防ぐ仕組み解明 Newspaper, magazine

    日経産業新聞（10面）  2011.7

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    多発性硬化症　悪化防ぐ仕組み解明

  • 多発性硬化症　カルシウム不足で悪化 Newspaper, magazine

    読売新聞（14面）  2011.6

    　More details

    多発性硬化症　カルシウム不足で悪化

  • アレルギー発症に関与　新たんぱく質発見 Newspaper, magazine

    読売新聞（2面）  2007.12

    　More details

    アレルギー発症に関与　新たんぱく質発見

  • 『アレルギーの元』引き込む細胞内たんぱく質 Newspaper, magazine

    毎日新聞（夕刊1面）  2007.12

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    『アレルギーの元』引き込む細胞内たんぱく質

  • タンパク質STIM1 アレルギー反応を制御 Newspaper, magazine

    科学新聞（6面）  2007.12

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    タンパク質STIM1 アレルギー反応を制御

  • アレルギー起こすたんぱく質を発見 Newspaper, magazine

    朝日新聞（夕刊2面）  2007.12

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    アレルギー起こすたんぱく質を発見

  • アレルギー発症の原因　たんぱく質特定 Newspaper, magazine

    日経産業新聞（8面）  2007.12

    　More details

    アレルギー発症の原因　たんぱく質特定

  • アレルギー原因たんぱく質解明 Newspaper, magazine

    日本経済新聞（19面）  2007.12

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    アレルギー原因たんぱく質解明

  • アレルギー反応誘発　必須たんぱく質発見 Newspaper, magazine

    日刊工業新聞（19面）  2007.12

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    アレルギー反応誘発　必須たんぱく質発見

  • アレルギー反応の制御因子　たん白質『STIM1』特定 Newspaper, magazine

    化学工業日報  2007.12

    　More details

    アレルギー反応の制御因子　たん白質『STIM1』特定

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Activities contributing to policy formation, academic promotion, etc.

  • 2023.8   日本免疫学会

    免疫サマースクール

Travel Abroad

  • 2002.4 - 2005.5

    Staying countory name 1：United States   Staying institution name 1：Oklahoma Medical Research Foundation, Cancer & Immunobiology Program