Regulatory roles of HIF-1a and glycolysis in autoimmunity
| Project/Area Number |
24591454
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
膠原病・アレルギー・感染症内科学
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| Research Institution | Dokkyo Medical University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
HASHIGUCHI Masaaki 獨協医科大学, 医学部, 准教授 (20372443)
KASHIWAKURA Yuji 獨協医科大学, 医学部, 助教 (40382890)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 自己免疫 / HIF-1a / 解糖系 / B細胞分化 / HIF-1α / 制御性T細胞 |
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| Outline of Final Research Achievements |
In order to understand the pathophysiology of HIF-1α/RAG-2–deficient chimeric mice, which develop autoimmunity resembling human systemic erythematosus, we analyzed mice with conditional knock-outs in HIF-1α in B cells and revealed that autoantibody production is regulated by HIF-1α in the very early stages of B cell development and/or HIF-1α in cells other than B cells. Although HIF-1α/RAG-2–deficient chimeric mice have increased regulatory T cells, we found that regulatory T cells less depend on glycolysis and need CD2-mediated down-regulation of pro-apoptotic Bim for their survival.
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Report
(4 results)
Research Products
(12 results)
