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Koizumi Shin-ichi Last modified date：2023.06.27

Assistant Professor / Research Center for Systems Immunology
Medical Institute of Bioregulation




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Homepage
https://kyushu-u.pure.elsevier.com/en/persons/shinichi-koizumi
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Phone
092-642-6973
Fax
092-6942-6972
Academic Degree
Doctor of Medical Science
Country of degree conferring institution (Overseas)
No
Field of Specialization
Immunology
Total Priod of education and research career in the foreign country
00years00months
Research
Research Interests
  • Fibroblasts are very major components of connective tissue. Although they are described in textbook terms as being involved in tissue maintenance, repair, and inflammation, their immunological importance in vivo has been little advanced for a long time. In recent years, the immunological importance of fibroblasts has been vigorously pursued by some researchers, who have reported that they play a central role in arthritis, acute kidney injury, and autoimmune dermatitis, as well as in aiding cancer progression and promoting tumor immune responses. Surprisingly, however, much remains to be clarified regarding acute lung injury caused by excessive immune system activation by viruses and how they are involved in the establishment of immune memory. Therefore, we are studying how fibroblasts function in the biological response to viral infection.
    keyword : Fibroblast, Immune response, Virus infection, Chemokine production, Tertiary lymphoid structure
    2020.09～2025.03.
Academic Activities
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1. Shin-ichi Koizumi, Horoki Ishikawa, JunB regulates homeostasis and suppressive functions of effector regulatory T cells, 日本免疫学会, 2018.12, Foxp3-expressing CD4+ regulatory T (Treg) cells need to differentiate into effector Treg (eTreg) cells to maintain immune homeostasis. T-cell receptor (TCR)-dependent induction of the transcription factor IRF4 is essential for eTreg differentiation, but how IRF4 activity is regulated in Treg cells is still unclear. Here we show that the AP-1 transcription factor, JunB, is expressed in eTreg cells and promotes an IRF4-dependent transcription program. Mice lacking JunB in Treg cells develop multi-organ autoimmunity, concomitant with aberrant activation of T helper cells. JunB promotes expression of Treg effector molecules, such as ICOS and CTLA4, in BATF-dependent and BATF-independent manners, and is also required for homeostasis and suppressive functions of eTreg. Mechanistically, JunB facilitates the accumulation of IRF4 at a subset of IRF4 target sites, including those located near Icos and Ctla4. Thus, JunB is a critical regulator of IRF4-dependent Treg effector programs, highlighting important functions for AP-1 in Treg-mediated immune homeostasis..


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