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Masuda Takahiro Last modified date:2023.01.06

Professor / Division of Molecular Neuroinflammation
Medical Research Center for High Depth Omics
Medical Institute of Bioregulation

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 Reseacher Profiling Tool Kyushu University Pure
Academic Degree
Country of degree conferring institution (Overseas)
Field of Specialization
neuroimmunology, pharmacology
ORCID(Open Researcher and Contributor ID)
Total Priod of education and research career in the foreign country
Research Interests
  • Understanding the nature of CNS macrophages
    keyword : microglia, CAMs, central nervous system
Academic Activities
1. Masuda T, Amann L, Prinz M, Novel insights into the origin and development of CNS macrophage subsets, Clin Transl Med, 2022.11.
2. Paolicelli RC, Sierra A, Stevens B, Tremblay ME, Aguzzi A, Ajami B, Amit I, Audinat E, Bechmann I, Bennett M, Bennett F, Bessis A, Biber K, Bilbo S, Blurton-Jones M, Boddeke E, Brites D, Brône B, Brown GC, Butovsky O, Carson MJ, Castellano B, Colonna M, Cowley SA, Cunningham C, Davalos D, De Jager PL, de Strooper B, Denes A, Eggen BJL, Eyo U, Galea E, Garel S, Ginhoux F, Glass CK, Gokce O, Gomez-Nicola D, González B, Gordon S, Graeber MB, Greenhalgh AD, Gressens P, Greter M, Gutmann DH, Haass C, Heneka MT, Heppner FL, Hong S, Hume DA, Jung S, Kettenmann H, Kipnis J, Koyama R, Lemke G, Lynch M, Majewska A, Malcangio M, Malm T, Mancuso R, Masuda T, Matteoli M, McColl BW, Miron VE, Molofsky AV, Monje M, Mracsko E, Nadjar A, Neher JJ, Neniskyte U, Neumann H, Noda M, Peng B, Peri F, Perry VH, Popovich PG, Pridans C, Priller J, Prinz M, Ragozzino D, Ransohoff RM, Salter MW, Schaefer A, Schafer DP, Schwartz M, Simons M, Smith CJ, Streit WJ, Tay TL, Tsai LH, Verkhratsky A, von Bernhardi R, Wake H, Wittamer V, Wolf SA, Wu LJ, Wyss-Coray T, Microglia states and nomenclature: A field at its crossroads, Neuron, 10.1016/j.neuron.2022.10.020., 2022.11.
3. Prinz M, Masuda T, Wheeler MA, Quintana FJ, Microglia and Central Nervous System-Associated Macrophages-From Origin to Disease Modulation, Annual Review of Immunology, 10.1146/annurev-immunol-093019-110159, 2021.04.
4. Masuda T, Sankowski R, Staszewski O, Prinz M, Microglia Heterogeneity in the Single-Cell Era, Cell Reports, doi: 10.1016/j.celrep.2020.01.010., 30(5):1271-1281, 2020.02.
5. Kierdorf K, Masuda T, Jordao M, Prinz M, Macrophages at CNS interfaces: ontogeny and function in health and disease, Nature Reviews Neuroscience, DOI: 10.1038/s41583-019-0201-x, 20(9):547-562, 2019.09.
1. Masuda T, Amann L, Monaco G, Sankowski R, Staszewski O, Krueger M, Del Gaudio F, He L, Paterson N, Nent E, Fernández-Klett F, Yamasaki A, Frosch M, Fliegauf M, Bosch LFP, Ulupinar H, Hagemeyer N, Schreiner D, Dorrier C, Tsuda M, Grothe C, Joutel A, Daneman R, Betsholtz C, Lendahl U, Knobeloch KP, Lämmermann T, Priller J, Kierdorf K, Prinz M, Specification of CNS macrophage subsets occurs postnatally in defined niches, Nature, 10.1038/s41586-022-04596-2, 604, 7907, 740-748, 2022.04, All tissue-resident macrophages of the central nervous system (CNS)-including parenchymal microglia, as well as CNS-associated macrophages (CAMs1) such as meningeal and perivascular macrophages2-7-are part of the CNS endogenous innate immune system that acts as the first line of defence during infections or trauma2,8-10. It has been suggested that microglia and all subsets of CAMs are derived from prenatal cellular sources in the yolk sac that were defined as early erythromyeloid progenitors11-15. However, the precise ontogenetic relationships, the underlying transcriptional programs and the molecular signals that drive the development of distinct CAM subsets in situ are poorly understood. Here we show, using fate-mapping systems, single-cell profiling and cell-specific mutants, that only meningeal macrophages and microglia share a common prenatal progenitor. By contrast, perivascular macrophages originate from perinatal meningeal macrophages only after birth in an integrin-dependent manner. The establishment of perivascular macrophages critically requires the presence of arterial vascular smooth muscle cells. Together, our data reveal a precisely timed process in distinct anatomical niches for the establishment of macrophage subsets in the CNS..
2. Kohno K, Shirasaka R, Yoshihara K, Mikuriya S, Tanaka K, Takanami K, Inoue K, Sakamoto H, Ohkawa Y, Masuda T, Tsuda M, A spinal microglia population involved in remitting and relapsing neuropathic pain, Science, 10.1126/science.abf6805, 376, 6588, 86-90, 376(6588):86-90, 2022.04, Neuropathic pain is often caused by injury and diseases that affect the somatosensory system. Although pain development has been well studied, pain recovery mechanisms remain largely unknown. Here, we found that CD11c-expressing spinal microglia appear after the development of behavioral pain hypersensitivity following nerve injury. Nerve-injured mice with spinal CD11c+ microglial depletion failed to recover spontaneously from this hypersensitivity. CD11c+ microglia expressed insulin-like growth factor-1 (IGF1), and interference with IGF1 signaling recapitulated the impairment in pain recovery. In pain-recovered mice, the depletion of CD11c+ microglia or the interruption of IGF1 signaling resulted in a relapse in pain hypersensitivity. Our findings reveal a mechanism for the remission and recurrence of neuropathic pain, providing potential targets for therapeutic strategies..
3. Masuda T, Iwamoto S, Yoshinaga R, Tozaki-Saitoh H, Nishiyama A, Mak TW, Tamura T, Tsuda M, Inoue K, Transcription factor IRF5 drives P2X4R+-reactive microglia gating neuropathic pain., Nature communications, 10.1038/ncomms4771, 5, 2014.05, In response to neuronal injury or disease, microglia adopt distinct reactive phenotypes via the expression of different sets of genes. Spinal microglia expressing the purinergic P2X4 receptor (P2X4R) after peripheral nerve injury (PNI) are implicated in neuropathic pain. Here we show that interferon regulatory factor-5 (IRF5), which is induced in spinal microglia after PNI, is responsible for direct transcriptional control of P2X4R. Upon stimulation of microglia by fibronectin, IRF5 induced de novo expression of P2X4R by directly binding to the promoter region of the P2rx4 gene. Mice lacking Irf5 did not upregulate spinal P2X4R after PNI, and also exhibited substantial resistance to pain hypersensitivity. Furthermore, we found that expression of IRF5 in microglia is regulated by IRF8. Thus, an IRF8-IRF5 transcriptional axis may contribute to shifting spinal microglia toward a P2X4R-expressing reactive state after PNI. These results may provide a new target for treating neuropathic pain..
1. Takahiro Masuda, Diversity and plasticity of microglia in mice and human, 第50回 日本免疫学会学術集会, 2021.12.
2. Takahiro Masuda, Single-cell analysis reveals spatial and temporal heterogeneity of microglia in human and mice, 第63回日本神経化学会大会, 2020.09.
Membership in Academic Society
  • Japanese Society for Immunology
  • The Pharmaceutical Society of Japan
  • Japanese Association for Study of Pain
  • The Japanese Society of Neurochemistry
  • The Japanese Pharmacological Society