The analysis of development of autoimmune disease and abnormalexpansion of B-1 cells in G5PR transgenic mice
| Project/Area Number |
23791116
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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 |
膠原病・アレルギー・感染症内科学
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| Research Institution | Kumamoto University |
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Principal Investigator |
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 膠原病学 / 自己免疫疾患 / B-1 細胞 / 抗原受容体シグナル / 免疫学 / B-1細胞 |
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| Research Abstract |
In the autoimmune disease, auto-reactive B cells are activated and produce theautoantibodies, which induce the tissue injury. We found that abnormal expression of G5PR,one of the B’’ regulatory subunit of the serine/threonine protein phosphatase 2A,induced the expansion of B-1a cells in the peritoneal cavity and generation ofautoantibodies in mice. Over-expression of G5PR in B-1a cells suppressed the JNK-mediatedapoptotic signal pathway and rescued from activation-induced cell death by antigenstimulation. These results suggest that G5PR may play a pivotal role in B cell selectionfor B-1a cells and in the development of autoimmune disease.
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Report
(3 results)
Research Products
(11 results)
