2024/10/04 更新

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写真a

ヤマムラ カズヒコ
山村 和彦
YAMAMURA KAZUHIKO
所属
九州大学病院 油症ダイオキシン研究診療センター 助教
職名
助教
外部リンク

受賞

  • Best Presentation Award

    2017年12月  

  • 2016年度九州大学医学博士優秀賞

    2017年3月   九州大学  

  • 安江賞

    2015年10月   第40回 東海皮膚科漢方研究会   ANTI-ALLERGIC MECHANISMS OF JAPANESE HERBAL MEDICINE, YOKUKANSAN ON MAST CELLS

  • 最優秀口演賞

    2014年7月   第17回生医研リトリート  

論文

  • Editorial: Crosstalk: skin cells and immune cells in inflammatory skin diseases

    Yamamura, K; Kim, HJ; Kim, JE

    FRONTIERS IN IMMUNOLOGY   15   1472313   2024年8月   ISSN:1664-3224

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    記述言語:英語   出版者・発行元:Frontiers in Immunology  

    DOI: 10.3389/fimmu.2024.1472313

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  • Evolution of pathologic B-cell subsets and serum environment-specific sIgEs in patients with atopic dermatitis and controls, from infancy to adulthood

    Czarnowicki, T; David, E; Yamamura, K; Han, J; He, H; Pavel, AB; Glickman, J; Erickson, T; Estrada, Y; Krueger, JG; Rangel, SM; Paller, AS; Guttman-Yassky, E

    ALLERGY   2024年7月   ISSN:0105-4538 eISSN:1398-9995

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    記述言語:英語   出版者・発行元:Allergy: European Journal of Allergy and Clinical Immunology  

    Background: While B-cells have historically been implicated in allergy development, a growing body of evidence supports their role in atopic dermatitis (AD). B-cell differentiation across ages in AD, and its relation to disease severity scores, has not been well defined. Objective: To compare the frequency of B-cell subsets in blood of 0–5, 6–11, 12–17, and ≥18 years old patients with AD versus age-matched controls. Methods: Flow cytometry was used to measure B-cell subset frequencies in the blood of 27 infants, 17 children, 11 adolescents, and 31 adults with moderate-to-severe AD and age-matched controls. IgD/CD27 and CD24/CD38 core gating systems and an 11-color flow cytometry panel were used to determine frequencies of circulating B-cell subsets. Serum total and allergen-specific IgE (sIgEs) levels were measured using ImmunoCAP®. Results: Adolescents with AD had lower frequencies of major B-cells subsets (p <.03). CD23 expression increased with age and was higher in AD compared to controls across all age groups (p <.04). In AD patients, multiple positive correlations were observed between IL-17-producing T-cells and B-cell subsets, most significantly non-switched memory (NSM) B-cells (r =.41, p =.0005). AD severity positively correlated with a list of B-cell subsets (p <.05). IL-9 levels gradually increased during childhood, reaching a peak in adolescence, paralleling allergen sensitization, particularly in severe AD. Principal component analysis of the aggregated environmental sIgE data showed that while controls across all ages tightly clustered together, adolescents with AD demonstrated distinct clustering patterns relative to controls. Conclusions: Multiple correlations between B-cells and T-cells, as well as disease severity measures, suggest a complex interplay of immune pathways in AD. Unique B-cell signature during adolescence, with concurrent allergen sensitization and IL-9 surge, point to a potentially wider window of opportunity to implement interventions that may prevent the progression of the atopic march.

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  • Difamilast, a Topical Phosphodiesterase 4 Inhibitor, Produces Soluble ST2 via the AHR-NRF2 Axis in Human Keratinocytes

    Tsuji, G; Yumine, A; Kawamura, K; Takemura, M; Kido-Nakahara, M; Yamamura, K; Nakahara, T

    INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES   25 ( 14 )   2024年7月   ISSN:1661-6596 eISSN:1422-0067

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    記述言語:英語   出版者・発行元:International Journal of Molecular Sciences  

    Difamilast, a phosphodiesterase 4 (PDE4) inhibitor, has been shown to be effective in the treatment of atopic dermatitis (AD), although the mechanism involved remains unclear. Since IL-33 plays an important role in the pathogenesis of AD, we investigated the effect of difamilast on IL-33 activity. Since an in vitro model of cultured normal human epidermal keratinocytes (NHEKs) has been utilized to evaluate the pharmacological potential of adjunctive treatment of AD, we treated NHEKs with difamilast and analyzed the expression of the suppression of tumorigenicity 2 protein (ST2), an IL-33 receptor with transmembrane (ST2L) and soluble (sST2) isoforms. Difamilast treatment increased mRNA and protein levels of sST2, a decoy receptor suppressing IL-33 signal transduction, without affecting ST2L expression. Furthermore, supernatants from difamilast-treated NHEKs inhibited IL-33-induced upregulation of TNF-α, IL-5, and IL-13 in KU812 cells, a basophil cell line sensitive to IL-33. We also found that difamilast activated the aryl hydrocarbon receptor (AHR)–nuclear factor erythroid 2-related factor 2 (NRF2) axis. Additionally, the knockdown of AHR or NRF2 abolished the difamilast-induced sST2 production. These results indicate that difamilast treatment produces sST2 via the AHR–NRF2 axis, contributing to improving AD symptoms by inhibiting IL-33 activity.

    DOI: 10.3390/ijms25147910

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  • 特発性多中心性Castleman 病に合併した難治性下腿潰瘍の 1 例

    杉 悠太, 山村 和彦, 竹井 樹, 中原 真希子, 一木 稔生, 宮脇 恒太, 山元 英嵩, 山村 美華, 中原 剛士

    西日本皮膚科   86 ( 3 )   233 - 237   2024年6月   ISSN:03869784 eISSN:18804047

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    記述言語:日本語   出版者・発行元:日本皮膚科学会西部支部  

    <p>47 歳,男性。約 2 年前より左下腿に潰瘍が出現し,拡大傾向であったため約 1 年前に前医を受診した。 外用治療を行われるも難治であり,潰瘍は徐々に拡大したため当科を紹介され受診し,精査加療目的に入院となった。入院時,左下腿の腫脹とほぼ全周にわたる潰瘍に加え,発熱,全身倦怠感,貧血,低栄養を認めた。背景の基礎疾患を検索したところ,血清 IL-6 値の上昇と CT 検査上,左鼠径部から傍大動脈周囲にかけて多発するリンパ節腫大を認めた。左鼠径部リンパ節生検を施行したところ,病理組織学的に硝子血管型 Castleman 病が疑われ,ほかの所見と合わせて特発性多中心性 Castleman 病と診断した。プレドニゾロン(PSL)15 mg/ 日の内服を開始し,発熱と全身倦怠感は改善傾向となった。潰瘍に対しては感染のコントロールを行い,デブリードマンおよび分層植皮術を施行した。2 回の分層植皮術と局所の圧迫,外用治療で潰瘍はほぼ上皮化し,PSL は徐々に減量した。Castleman 病と下腿潰瘍の合併は比較的稀ではあるが,全身症状を伴う難治性の下腿潰瘍に対しては本症を疑う必要があると考えた。</p>

    DOI: 10.2336/nishinihonhifu.86.233

    CiNii Research

  • Gram-negative anaerobes elicit a robust keratinocytes immune response with potential insights into HS pathogenesis

    Williams S.C., Garcet S., Hur H., Miura S., Gonzalez J., Navrazhina K., Yamamura-Murai M., Yamamura K., Li X., Frew J., Fischetti V.A., Sela U., Krueger J.G.

    Experimental Dermatology   33 ( 5 )   2024年4月   ISSN:0906-6705 eISSN:1600-0625

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    掲載種別:研究論文(学術雑誌)   出版者・発行元:Experimental Dermatology  

    Hidradenitis Suppurativa (HS) is a chronic autoinflammatory skin disease with activated keratinocytes, tunnel formation and a complex immune infiltrate in tissue. The HS microbiome is polymicrobial with an abundance of commensal gram-positive facultative (GPs) Staphylococcus species and gram-negative anaerobic (GNA) bacteria like Prevotella, Fusobacterium and Porphyromonas with increasing predominance of GNAs with disease severity. We sought to define the keratinocyte response to bacteria commonly isolated from HS lesions to probe pathogenic relationships between HS and the microbiome. Type strains of Prevotella nigrescens, Prevotella melaninogenica, Prevotella intermedia, Prevotella asaccharolytica, Fusobacterium nucleatum, as well as Staphylococcus aureus and the normal skin commensal Staphylococcus epidermidis were heat-killed and co-incubated with normal human keratinocytes. RNA was collected and analysed using RNAseq and RT-qPCR. The supernatant was collected from cell culture for protein quantification. Transcriptomic profiles between HS clinical samples and stimulated keratinocytes were compared. Co-staining of patient HS frozen sections was used to localize bacteria in lesions. A mouse intradermal injection model was used to investigate early immune recruitment. TLR4 and JAK inhibitors were used to investigate mechanistic avenues of bacterial response inhibition. GNAs, especially F. nucleatum, stimulated vastly higher CXCL8, IL17C, CCL20, IL6, TNF and IL36γ transcription in normal skin keratinocytes than the GPs S. epidermidis and S. aureus. Using RNAseq, we found that F. nucleatum (and Prevotella) strongly induced the IL-17 pathway in keratinocytes and overlapped with transcriptome profiles of HS patient clinical samples. Bacteria were juxtaposed to activated keratinocytes in vivo, and F. nucleatum strongly recruited murine neutrophil and macrophage migration. Both the TLR4 and pan-JAK inhibitors reduced cytokine production. Detailed transcriptomic profiling of healthy skin keratinocytes exposed to GNAs prevalent in HS revealed a potent, extensive inflammatory response vastly stronger than GPs. GNAs stimulated HS-relevant genes, including many genes in the IL-17 response pathway, and were significantly associated with HS tissue transcriptomes. The close association of activated keratinocytes with bacteria in HS lesions and innate infiltration in murine skin cemented GNA pathogenic potential. These novel mechanistic insights could drive future targeted therapies.

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  • The Therapeutic Aryl Hydrocarbon Receptor-Modulating Agent Tapinarof Regulates SEMA3A Expression in Human Keratinocytes through NRF2 国際誌

    Tsuji, G; Yumine, A; Yamamura, K; Takemura, M; Nakahara, MK; Ito, T; Nakahara, T

    JOURNAL OF INVESTIGATIVE DERMATOLOGY   144 ( 3 )   710 - 713.e8   2024年3月   ISSN:0022-202X eISSN:1523-1747

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:Journal of Investigative Dermatology  

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  • Regulatory Mechanism of the IL-33-IL-37 Axis via Aryl Hydrocarbon Receptor in Atopic Dermatitis and Psoriasis 国際誌

    Tsuji, G; Yamamura, K; Kawamura, K; Kido-Nakahara, M; Ito, T; Nakahara, T

    INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES   24 ( 19 )   2023年10月   ISSN:1661-6596 eISSN:1422-0067

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:International Journal of Molecular Sciences  

    Interleukin (IL)-33 and IL-37 have been identified as novel cytokines involved in various inflammatory diseases. However, their specific roles remain largely unknown. Recent studies have shown that IL-33, which triggers inflammation, and IL-37, which suppresses it, cooperatively regulate the balance between inflammation and anti-inflammation. IL-33 and IL-37 are also deeply involved in the pathogenesis of inflammatory skin diseases such as atopic dermatitis (AD) and psoriasis. Furthermore, a signaling pathway by which aryl hydrocarbon receptor (AHR), a receptor for dioxins, regulates the expression of IL-33 and IL-37 has been revealed. Here, we outline recent findings on the mechanisms regulating IL-33 and IL-37 expression in AD and psoriasis. IL-33 expression is partially dependent on mitogen-activated protein kinase (MAPK) activation, and IL-37 has a role in suppressing MAPK in human keratinocytes. Furthermore, IL-33 downregulates skin barrier function proteins including filaggrin and loricrin, thereby downregulating the expression of IL-37, which colocalizes with these proteins. This leads to an imbalance of the IL-33–IL-37 axis, involving increased IL-33 and decreased IL-37, which may be associated with the pathogenesis of AD and psoriasis. Therefore, AHR-mediated regulation of the IL-33–IL-37 axis may lead to new therapeutic strategies for the treatment of AD and psoriasis.

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  • Staphylococcus Aureus and Streptococcus Pyogenes Induce Psoriasis-Related Transcriptomes Augmented by IL-17A and TNF-α. 国際誌

    Miura S., Ichimura Y., Sela U., Garcet S., Salud-Gnilo C., Li X., Gonzalez J., Murai-Yamamura M., Yamamura K., Rambhia D., Kunjravia N., Krueger J.G.

    Journal of Investigative Dermatology   143 ( 8 )   1613 - 1617   2023年8月   ISSN:0022202X

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:Journal of Investigative Dermatology  

    DOI: 10.1016/j.jid.2022.12.026

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  • Cathelicidin Antimicrobial Peptide LL37 Induces Toll-Like Receptor 8 and Amplifies IL-36γ and IL-17C in Human Keratinocytes. 国際誌

    Miura S., Garcet S., Li X., Cueto I., Salud-Gnilo C., Kunjravia N., Yamamura K., Gonzalez J., Murai-Yamamura M., Rambhia D., Krueger J.G.

    Journal of Investigative Dermatology   143 ( 5 )   832 - 841   2023年5月   ISSN:0022202X

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:Journal of Investigative Dermatology  

    LL37 is produced by skin injury and bacterial infection and plays an important role in the early stages of psoriasis. In particular, the intracellular receptors toll-like receptors (TLR)3, TLR7, TLR8, and TLR9 are thought to be involved in the pathogenesis of psoriasis in conjunction with LL37, but the interaction between TLR7/8 and LL37 in keratinocytes (KCs) remains unclear. This study aimed to clarify the relationship between LL37 and TLR7/8 in KCs and their involvement in the pathogenetic pathways seen in psoriasis using cultured KCs and skin samples of patients with psoriasis. TLR7/8 was induced by LL37 in KCs. TLR8 but not TLR7 functionally induced many psoriasis-related molecules, whereas IL-17C was not altered by the blockade of TLR7/8. Although costimulation of LL37 with self-RNA/DNA did not show any interaction, LL37 itself would promote psoriasis-related genes. IL-36 receptor antagonistic antibody suppressed IL-17C induced by LL37. In psoriatic epidermis, LL37, TLRs, IL-17C, and IL-36γ expressions were increased and coexpressed with each other. Thus, we concluded that LL37 activates TLR8 in KCs and induces IL-17C through the induction of IL-36γ. Regulation of TLR8 or LL37 in KCs could be a potential therapeutic strategy for psoriatic inflammation.

    DOI: 10.1016/j.jid.2022.10.017

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  • PDE4 inhibition by difamilast regulates filaggrin and loricrin expression via keratinocyte proline-rich protein in human keratinocytes 国際誌

    Tsuji, G; Hashimoto-Hachiya, A; Yumine, A; Takemura, M; Kido-Nakahara, M; Ito, T; Yamamura, K; Nakahara, T

    JOURNAL OF DERMATOLOGICAL SCIENCE   110 ( 2 )   61 - 68   2023年5月   ISSN:0923-1811 eISSN:1873-569X

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:Journal of Dermatological Science  

    BACKGROUND: Difamilast, a topical phosphodiesterase 4 (PDE4) inhibitor, has been shown to be effective for treating atopic dermatitis (AD), but the molecular mechanism involved is unclear. Since skin barrier dysfunction including reduced expression of filaggrin (FLG) and loricrin (LOR) contributes to AD development, difamilast treatment may be able to improve this dysfunction. PDE4 inhibition increases transcriptional activity of cAMP-responsive element binding protein (CREB). Therefore, we hypothesized that difamilast may affect FLG and LOR expression via CREB in human keratinocytes. OBJECTIVE: To elucidate the mechanism by which difamilast regulates FLG and LOR expression via CREB in human keratinocytes. METHODS: We analyzed normal human epidermal keratinocytes (NHEKs) treated with difamilast. RESULTS: We observed increases of intracellular cAMP levels and CREB phosphorylation in difamilast (5 μM)-treated NHEKs. Next, we found that difamilast treatment increased mRNA and protein levels of FLG and LOR in NHEKs. Since reduced expression of keratinocyte proline-rich protein (KPRP) is reported to be involved in skin barrier dysfunction in AD, we examined KPRP expression in difamilast-treated NHEKs. We found that difamilast treatment increased mRNA and protein levels of KPRP in NHEKs. Furthermore, KPRP knockdown using siRNA transfection abolished the upregulation of FLG and LOR in difamilast-treated NHEKs. Finally, CREB knockdown canceled the upregulation of FLG, LOR, and KPRP in difamilast-treated NHEKs, indicating that PDE4 inhibition by difamilast treatment positively regulates FLG and LOR expression via the CREB-KPRP axis in NHEKs. CONCLUSION: These findings may provide further guidance for therapeutic strategies in the treatment of AD using difamilast.

    DOI: 10.1016/j.jdermsci.2023.04.007

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  • The role of OX40/OX40L axis in atopic dermatitis

    Yamamura, K; Yamamura, M; Garcet, S; Dahabreh, D; Gonzalez, J; Miura, S; Williams, S; Nakahara, T; Krueger, J; Guttman-Yassky, E

    JOURNAL OF INVESTIGATIVE DERMATOLOGY   143 ( 5 )   S11 - S11   2023年5月   ISSN:0022-202X eISSN:1523-1747

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  • Tapinarof, a therapeutic AHR-modulating agent, induces semaphorin 3A production via NRF2 in human keratinocytes: Implications for atopic dermatitis

    Tsuji, G; Takai-Yumine, A; Takemura, M; Yamamura, K; Ito, T; Kido-Nakahara, M; Nakahara, T

    JOURNAL OF INVESTIGATIVE DERMATOLOGY   143 ( 5 )   S189 - S189   2023年5月   ISSN:0022-202X eISSN:1523-1747

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  • PDE4 inhibition by difamilast regulates filaggrin and loricrin expression via keratinocyte proline-rich protein in human keratinocytes(タイトル和訳中)

    Tsuji Gaku, Hashimoto-Hachiya Akiko, Yumine Ayako, Takemura Masaki, Kido-Nakahara Makiko, Ito Takamichi, Yamamura Kazuhiko, Nakahara Takeshi

    Journal of Dermatological Science   110 ( 2 )   61 - 68   2023年5月   ISSN:0923-1811

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    記述言語:英語   出版者・発行元:エルゼビア・ジャパン(株)  

  • Novel Therapeutic Targets for the Treatment of Atopic Dermatitis 国際誌

    Tsuji, G; Yamamura, K; Kawamura, K; Kido-Nakahara, M; Ito, T; Nakahara, T

    BIOMEDICINES   11 ( 5 )   2023年4月   ISSN:2227-9059 eISSN:2227-9059

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:Biomedicines  

    Atopic dermatitis (AD) is a chronic inflammatory skin disease that significantly impacts quality of life. The pathogenesis of AD is a complex combination of skin barrier dysfunction, type II immune response, and pruritus. Progress in the understanding of the immunological mechanisms of AD has led to the recognition of multiple novel therapeutic targets. For systemic therapy, new biologic agents that target IL-13, IL-22, IL-33, the IL-23/IL-17 axis, and OX40-OX40L are being developed. Binding of type II cytokines to their receptors activates Janus kinase (JAK) and its downstream signal, namely signal transduction and activator of transcription (STAT). JAK inhibitors block the activation of the JAK-STAT pathway, thereby blocking the signaling pathways mediated by type II cytokines. In addition to oral JAK inhibitors, histamine H4 receptor antagonists are under investigation as small-molecule compounds. For topical therapy, JAK inhibitors, aryl hydrocarbon receptor modulators, and phosphodiesterase-4 inhibitors are being approved. Microbiome modulation is also being examined for the treatment of AD. This review outlines current and future directions for novel therapies of AD that are currently being investigated in clinical trials, focusing on their mechanisms of action and efficacy. This supports the accumulation of data on advanced treatments for AD in the new era of precision medicine.

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  • Identification of a functional <i>DOCK8</i> gene polymorphism associated with atopic dermatitis 国際誌

    Kunimura, K; Yamamura, K; Nakahara, T; Kido-Nakahara, M; Uruno, T; Fukui, Y

    ALLERGY   77 ( 12 )   3670 - 3672   2022年12月   ISSN:0105-4538 eISSN:1398-9995

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    記述言語:英語   出版者・発行元:Allergy: European Journal of Allergy and Clinical Immunology  

    DOI: 10.1111/all.15429

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  • The Dawn of a New Era in Atopic Dermatitis Treatment 国際誌

    Yamamura, K; Nakahara, T

    JOURNAL OF CLINICAL MEDICINE   11 ( 20 )   2022年10月   ISSN:2077-0383 eISSN:2077-0383

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:Journal of Clinical Medicine  

    Atopic dermatitis (AD) is one of the most common chronic inflammatory skin diseases, and the condition is typified by barrier dysfunction and immune dysregulation. Recent studies have characterized various phenotypes and endotypes of AD and elucidated the mechanism. Numerous topical and systemic narrow targeting therapies for AD have been developed according to these findings. Topical medications, including Janus kinase (JAK) inhibitors, phosphodiesterase 4 inhibitors, and the aryl hydrocarbon receptor agonist tapinarof, are effective and safe for AD compared to topical corticosteroids. Oral JAK inhibitors and monoclonal antibodies targeting interleukin (IL)-4, IL-13, IL-31, IL-33, OX40, thymic stromal lymphopoietin, and sphingosine 1-phosphate signaling have displayed outstanding efficacy against moderate-to-severe AD. We are currently in a new era of AD treatment.

    DOI: 10.3390/jcm11206145

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  • Concordance in judgment of clinical borders of basal cell carcinomas in Japanese patients: A preliminary study of JCOG2005 (J-BASE-MARGIN)

    Kamimura, A; Nakamura, Y; Takenouchi, T; Matsushita, S; Omodaka, T; Yamamura, K; Uchi, H; Yoshikawa, S; Yanagisawa, H; Ito, T; Kiyohara, Y; Nakamura, Y; Aoki, M; Ishizuki, S; Oashi, K; Miyagawa, T; Maeda, T; Ogata, D; Hatta, N; Ohe, S; Isei, T; Takahashi, A; Umeda, Y; Yamaguchi, B; Ishikawa, M; Horimoto, K; Fujsawa, Y; Uehara, J; Shibayama, Y; Kiniwa, Y; Kawahara, Y; Matsuya, T; Uhara, H; Kato, J; Nakamura, Y; Murakami, T; Namikawa, K; Yoshino, K; Funakoshi, T; Takatsuka, S; Matsui, Y; Sasaki, J; Koga, H; Yokota, K; Komori, T; Fukushima, S; Yamazaki, N

    JOURNAL OF DERMATOLOGY   49 ( 9 )   837 - 844   2022年9月   ISSN:0385-2407 eISSN:1346-8138

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  • Confirmatory trial of narrower side margin excision for head and neck basal cell carcinoma in the Japanese (East Asian) population: JCOG2005 (J-BASE-MARGIN).

    Nakamura, Y; Sano, Y; Kataoka, T; Shibata, T; Fukuda, H; Matsushita, S; Fujisawa, Y; Takenouchi, T; Omodaka, T; Yamamura, K; Aoki, M; Uchi, H; Tsutsui, K; Yoshikawa, S; Ogata, D; Yanagisawa, H; Omatsu, J; Ito, T; Namikawa, K; Yamazaki, N

    JOURNAL OF CLINICAL ONCOLOGY   40 ( 16 )   2022年6月   ISSN:0732-183X eISSN:1527-7755

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  • TH 2 cytokines and Staphylococcus aureus cooperatively induce atopic dermatitis-like transcriptomes. 国際誌

    Mika Murai-Yamamura, Sandra Garcet, Kazuhiko Yamamura, Juana Gonzalez, Shunsuke Miura, Xuan Li, Hong Hur, Emma Guttman-Yassky, James G Krueger

    Allergy   76 ( 11 )   3534 - 3537   2021年11月

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    記述言語:英語  

    DOI: 10.1111/all.15035

  • IL-36 and IL-17A Cooperatively Induce a Psoriasis-Like Gene Expression Response in Human Keratinocytes. 国際誌

    141 ( 8 )   2086 - 2090   2021年8月

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    記述言語:英語  

    DOI: 10.1016/j.jid.2021.01.019

  • OVOL2-Mediated ZEB1 Downregulation May Prevent Promotion of Actinic Keratosis to Cutaneous Squamous Cell Carcinoma. 国際誌

    Maho Murata, Takamichi Ito, Yuka Tanaka, Kazuhiko Yamamura, Kazuhisa Furue, Masutaka Furue

    Journal of clinical medicine   9 ( 3 )   2020年2月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.3390/jcm9030618

  • Selective role of neurokinin B in IL-31-induced itch response in mice. 国際誌

    Daiji Sakata, Takehito Uruno, Keisuke Matsubara, Tsugunobu Andoh, Kazuhiko Yamamura, Yuki Magoshi, Kazufumi Kunimura, Yasuhisa Kamikaseda, Masutaka Furue, Yoshinori Fukui

    The Journal of allergy and clinical immunology   144 ( 4 )   1130 - 1133   2019年10月

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    記述言語:英語  

    DOI: 10.1016/j.jaci.2019.06.031

  • Serum squamous cell carcinoma antigen (SCCA)-2 correlates with clinical severity of pediatric atopic dermatitis in Ishigaki cohort. 国際誌

    Satoshi Takeuchi, Norihiro Furusyo, Junya Ono, Yoshinori Azuma, Masaki Takemura, Hitokazu Esaki, Kazuhiko Yamamura, Yasutaka Mitamura, Gaku Tsuji, Mari Kiyomatsu-Oda, Jun Hayashi, Kenji Izuhara, Masutaka Furue

    Journal of dermatological science   95 ( 2 )   70 - 75   2019年8月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.1016/j.jdermsci.2019.07.005

  • Cyto/chemokine profile of in vitro scratched keratinocyte model: Implications of significant upregulation of CCL20, CXCL8 and IL36G in Koebner phenomenon. 国際誌

    Kazuhisa Furue, Takamichi Ito, Yuka Tanaka, Ayako Yumine, Akiko Hashimoto-Hachiya, Masaki Takemura, Maho Murata, Kazuhiko Yamamura, Gaku Tsuji, Masutaka Furue

    Journal of dermatological science   94 ( 1 )   244 - 251   2019年4月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.1016/j.jdermsci.2019.04.002

  • Tryptophan photo-product FICZ upregulates AHR/MEK/ERK-mediated MMP1 expression: Implications in anti-fibrotic phototherapy. 国際誌

    Mika Murai, Kazuhiko Yamamura, Akiko Hashimoto-Hachiya, Gaku Tsuji, Masutaka Furue, Chikage Mitoma

    Journal of dermatological science   91 ( 1 )   97 - 103   2018年7月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.1016/j.jdermsci.2018.04.010

  • Cholesterol sulfate is a DOCK2 inhibitor that mediates tissue-specific immune evasion in the eye. 国際誌

    Tetsuya Sakurai, Takehito Uruno, Yuki Sugiura, Takaaki Tatsuguchi, Kazuhiko Yamamura, Miho Ushijima, Yuko Hattori, Mutsuko Kukimoto-Niino, Chiemi Mishima-Tsumagari, Mayuki Watanabe, Makoto Suematsu, Yoshinori Fukui

    Science signaling   11 ( 541 )   2018年7月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.1126/scisignal.aao4874

  • Highlighting Interleukin-36 Signalling in Plaque Psoriasis and Pustular Psoriasis. 国際誌

    Kazuhisa Furue, Kazuhiko Yamamura, Gaku Tsuji, Chikage Mitoma, Hiroshi Uchi, Takeshi Nakahara, Makiko Kido-Nakahara, Takafumi Kadono, Masutaka Furue

    Acta dermato-venereologica   98 ( 1 )   5 - 13   2018年1月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.2340/00015555-2808

  • The transcription factor EPAS1 links DOCK8 deficiency to atopic skin inflammation via IL-31 induction. 国際誌

    Kazuhiko Yamamura, Takehito Uruno, Akira Shiraishi, Yoshihiko Tanaka, Miho Ushijima, Takeshi Nakahara, Mayuki Watanabe, Makiko Kido-Nakahara, Ikuya Tsuge, Masutaka Furue, Yoshinori Fukui

    Nature communications   8   13946 - 13946   2017年1月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.1038/ncomms13946

  • Levels of immunoglobulin E specific to the major food allergen and chemokine (C-C motif) ligand (CCL)17/thymus and activation regulated chemokine and CCL22/macrophage-derived chemokine in infantile atopic dermatitis on Ishigaki Island. 国際誌

    Hitokazu Esaki, Satoshi Takeuchi, Norihiro Furusyo, Kazuhiko Yamamura, Sayaka Hayashida, Gaku Tsuji, Masaki Takemura, Jun Hayashi, Masutaka Furue

    The Journal of dermatology   43 ( 11 )   1278 - 1282   2016年11月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.1111/1346-8138.13360

  • Incidence, serum IgE and TARC/CCL17 levels in atopic dermatitis associated with other allergic diseases: an update from the Ishigaki cohort. 国際誌

    Satoshi Takeuchi, Hitokazu Esaki, Norihiro Furusyo, Sayaka Hayashida, Kazuhiko Yamamura, Gaku Tsuji, Masaki Takemura, Jun Hayashi, Masutaka Furue

    Acta dermato-venereologica   95 ( 4 )   480 - 4   2015年4月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.2340/00015555-1989

  • Anti-allergic mechanisms of Japanese herbal medicine, yokukansan on mast cells. 国際誌

    Kazuhiko Yamamura, Shiori Kato, Takahiro A Kato, Yoshito Mizoguchi, Akira Monji, Shigenobu Kanba, Masutaka Furue, Satoshi Takeuchi

    The Journal of dermatology   41 ( 9 )   808 - 14   2014年9月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.1111/1346-8138.12578

  • DOCK5 functions as a key signaling adaptor that links FcεRI signals to microtubule dynamics during mast cell degranulation. 国際誌

    Kana Ogawa, Yoshihiko Tanaka, Takehito Uruno, Xuefeng Duan, Yosuke Harada, Fumiyuki Sanematsu, Kazuhiko Yamamura, Masao Terasawa, Akihiko Nishikimi, Jean-François Côté, Yoshinori Fukui

    211 ( 7 )   1407 - 19   2014年6月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Mast cells play a key role in the induction of anaphylaxis, a life-threatening IgE-dependent allergic reaction, by secreting chemical mediators that are stored in secretory granules. Degranulation of mast cells is triggered by aggregation of the high-affinity IgE receptor, FcεRI, and involves dynamic rearrangement of microtubules. Although much is known about proximal signals downstream of FcεRI, the distal signaling events controlling microtubule dynamics remain elusive. Here we report that DOCK5, an atypical guanine nucleotide exchange factor (GEF) for Rac, is essential for mast cell degranulation. As such, we found that DOCK5-deficient mice exhibit resistance to systemic and cutaneous anaphylaxis. The Rac GEF activity of DOCK5 is surprisingly not required for mast cell degranulation. Instead, DOCK5 associated with Nck2 and Akt to regulate microtubule dynamics through phosphorylation and inactivation of GSK3β. When DOCK5-Nck2-Akt interactions were disrupted, microtubule formation and degranulation response were severely impaired. Our results thus identify DOCK5 as a key signaling adaptor that orchestrates remodeling of the microtubule network essential for mast cell degranulation.

    DOI: 10.1084/jem.20131926

  • Decrease of reactive oxygen species and reciprocal increase of nitric oxide in human dermal endothelial cells by Bidens pilosa extract: a possible explanation of its beneficial effect on livedo vasculopathy. 国際誌

    Futoshi Kohda, Masakazu Takahara, Akiko Hachiya, Kenjiro Takei, Gaku Tsuji, Kazuhiko Yamamura, Masutaka Furue

    Journal of dermatological science   72 ( 1 )   75 - 7   2013年10月

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    記述言語:英語  

    DOI: 10.1016/j.jdermsci.2013.05.008

  • Subcutaneous calcification of the lower legs in a patient with mixed connective tissue disease. 国際誌

    Kazuhiko Yamamura, Masakazu Takahara, Kana Masunaga, Takuya Sawabe, Masaki Kitano, Toshihiko Mashino, Masutaka Furue

    The Journal of dermatology   38 ( 8 )   791 - 3   2011年8月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.1111/j.1346-8138.2010.01177.x

▼全件表示

講演・口頭発表等

共同研究・競争的資金等の研究課題

  • アトピー性皮膚炎における新規そう痒惹起物質の同定とその感知機構の解明

    研究課題/領域番号:23K15285  2023年 - 2025年

    科学研究費助成事業  若手研究(A)

    山村 和彦

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    担当区分:研究代表者  資金種別:科研費

    本研究では、ヒト感覚神経細胞をこれまで報告のあったアトピー性皮膚炎患者血球細胞で発現が変化しているサイトカイン/生理活性脂質で刺激し、解析することで、アトピー性皮膚炎痒みに関わりのある新規そう痒惹起物質の同定、及びその産生制御機構とシグナル伝達経路の解明、新たな創薬標的の導出を目的とする。

    CiNii Research

  • iPS細胞由来ヒト感覚神経を用いたアトピー性皮膚炎における痒みのメカニズムの探求

    研究課題/領域番号:22K20686  2022年 - 2023年

    日本学術振興会  科学研究費助成事業  研究活動スタート支援

    山村 和彦

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    担当区分:研究代表者  資金種別:科研費

    アトピー性皮膚炎は国民の7-15%が罹患し、多くの患者さんが激しい痒みに悩まされています。これまでヒトの痒みに関連する研究は、ヒト末梢神経が入手困難だったこともあり、ほとんどなされてきませんでした。本研究は、近年開発されたヒトiPS細胞由来の末梢感覚神経を用いることで、アトピー性皮膚炎に特徴的な痒みを引き起こすメカニズムとそれに重要な物質を特定することを目的にしています。

    CiNii Research

  • 炎症性皮膚疾患のThサブセット偏移を制御する生理活性脂質の同定と疾患モデルの創出

    2020年 - 2022年

    日本学術振興会  海外特別研究員

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    担当区分:研究代表者  資金種別:共同研究

  • アトピー性皮膚炎における新しい共刺激分子の特徴と役割

    2018年 - 2019年

    アステラス病態代謝研究会

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    担当区分:研究代表者  資金種別:受託研究

海外渡航歴

  • 2018年11月 - 2022年3月

    滞在国名1:アメリカ合衆国   滞在機関名1:The Rockefeller University (USA), Laboratory for Investigative Dermatology