| Project/Area Number |
26860342
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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 |
Immunology
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| Research Institution | Okinawa Institute of Science and Technology Graduate University |
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Principal Investigator |
Ishikawa Hiroki 沖縄科学技術大学院大学, 免疫シグナルユニット, 准教授 (30648621)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | ヘルパーT細胞 / 転写制御 / 転写因子 / 自己免疫疾患 / Th17 |
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| Outline of Final Research Achievements |
CD4 T cells are a key player to mediate adaptive immune responses. Upon detection of the target antigen, naive CD4+ T cells differentiate into T helper (Th) subsets including Th1, Th2, and Th17 cells. Each of these Th subsets differentially controls protective immune responses against different pathogens as well as harmful immune responses leading to allergy and autoimmune diseases. Here we found that HLX1 expression was induced in Th17 cells as well as Th1 cells. HLX1 induction was mediated by STAT4 and STAT3 transcription factors in Th1 and Th17 cells, respectively. Th17-dependent experimental autoimmune encephalomyelitis (EAE) was ameliorated in the mice with HLX1-deficient T cells. Th1 and Th17 cells lacking HLX1 showed impaired expression of cell surface antigens whose signal has been shown to modulate T cell receptor signaling. These results suggest that HLX1-dependent regulation of gene expression is important in Th1 and Th17 differentiation and function.
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