Identification of mechanisms for IL-10 production by regulatory B cells
| Project/Area Number |
25860800
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Hematology
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| Research Institution | National Center for Global Health and Medicine |
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Principal Investigator |
Yamazaki Nao 国立研究開発法人国立国際医療研究センター, 免疫制御研究部, 上級研究員 (20646848)
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| Project Period (FY) |
2013-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2015: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | B細胞 / 形質細胞 / IL-10 / 免疫グロブリンクラススイッチ / 制御性B細胞 / IL-13 |
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| Outline of Final Research Achievements |
We have identified a new population of phenotypic IgM+B220loCD138hi cells responsible for marked IL-10 production in murine bone marrow and spleen. These cells predominantly secreted IgM and had characteristics of long-lived plasma cells. We found that IL-10 production was strongly correlated with the expression level of Prdm1 (encoding the Blimp-1 protein), an essential regulator of plasma cell development. Furthermore, transduction of Prdm1 induced Il10 expression in naive B cells. Immunoglobulin class-switching recombination events resulted in the downregulation of both Il10 and Prdm1 expression in differentiating B cells. Thus, the prolonged elevation of Blimp-1 expression during the formation of IgM+CD138hi cells without class-switching elicited IL-10 production. Adoptive transfer of Il10-deficient B cells into B cell-deficient mice demonstrated that IgM+CD138hi cell-derived IL-10 supported class-switched plasma cells and their antibody production in response to antigen challenge.
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Report
(5 results)
Research Products
(3 results)
