Dual roles of type I interferon-activated B cells and the effect on autoimmunity
| Project/Area Number |
18H02626
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Review Section |
Basic Section 49010:Pathological biochemistry-related
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| Research Institution | Kyushu University |
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Principal Investigator |
Baba Yoshihiro 九州大学, 生体防御医学研究所, 教授 (20415269)
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Project Status |
Completed (Fiscal Year 2020)
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| Budget Amount *help |
¥17,420,000 (Direct Cost: ¥13,400,000、Indirect Cost: ¥4,020,000)
Fiscal Year 2020: ¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2019: ¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2018: ¥6,500,000 (Direct Cost: ¥5,000,000、Indirect Cost: ¥1,500,000)
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| Keywords | B細胞 / インターフェロン / IL-10 / 自己免疫疾患 / 制御性B細胞 / I型インターフェロン |
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| Outline of Final Research Achievements |
Although type I interferon (IFN-I) is known to have the dual role of exacerbation and suppression of autoimmune diseases, its underlying molecular mechanism remain unclear. In this study, we addressed the issue by examining the B cell response to IFN-I. We showed that human B cells give rise to IL-10-producing plasmablasts by stimulating IFN-I, and revealed its properties. Furthermore, we found that the IL-10 plasmablasts inhibit T cell proliferation. We also showed that murine B cells respond to TLR agonists and IFN-I synergistically and cooperately to differentiate into IL-10-producing and non-producing plasmablasts.
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| Academic Significance and Societal Importance of the Research Achievements |
高齢化社会を迎えた先進国では自己免疫患者数の増加が大きな問題となっているが、その発症原因は不明であり、治療法も限定的である。制御性B細胞の分化がIFNで誘導されるという知見は、自己免疫疾患を抑制するB細胞を増幅させて治療に用いる方法に重要な情報となると考えられる。また、TLRアゴニストとIFN-Iのクロストークにより、自己免疫を増悪する抗体産生プラズマブラストから抑制するプラズマブラストへ分化の方向性を制御する可能性を示唆しており、プラズマ細胞分化の新規分子機構となることが期待される。
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Report
(4 results)
Research Products
(23 results)
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[Journal Article] Tet2 and Tet3 in B cells are required to repress CD86 and prevent autoimmunity2020
Author(s)
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, P. A. Raman, I. Li, Q. Z. Kubo, M. Fujiki, K. Nakato, R. Shirahige, K. Araki, H. Miura, F. Ito, T. Kawakami, E. Baba, Y. Kurosaki, T.
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Journal Title
Nature Immunology
Volume: 21
Issue: 8
Pages: 950-961
DOI
Related Report
Peer Reviewed / Open Access / Int'l Joint Research
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[Journal Article] GPR40 activation initiates store-operated Ca2+ entry and potentiates insulin secretion via the IP3R1/STIM1/Orai1 pathway in pancreatic β-cells2019
Author(s)
Usui R, Yabe D, Fauzi M, Goto H, Botagarova A, Tokumoto S, Tatsuoka H, Tahara Y, Kobayashi S, Manebe T, Baba Y, Kurosaki T, Herrera PL, Ogura M, Nagashima K, Inagaki N
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Journal Title
Sci Rep.
Volume: 9
Issue: 1
Pages: 15562-15562
DOI
Related Report
Peer Reviewed / Open Access / Int'l Joint Research
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