| Project/Area Number |
14599011
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
細胞死(アポトーシス)
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| Research Institution | AKITA UNIVERSITY |
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Principal Investigator |
OHTEKI Toshiaki Akita University, School of Medicine, Professor, 医学部, 教授 (50233200)
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| Project Period (FY) |
2002 – 2003
|
| Project Status |
Completed (Fiscal Year 2003)
|
| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2003: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2002: ¥2,600,000 (Direct Cost: ¥2,600,000)
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| Keywords | CTLA-4 / IL-2 / IL-2R / T cell activation / autoimmune disease / human / mouse / 活性化T細胞 / B7 / IL-15 / 抗原特異的 / in vivo / ホメオスターシス増殖 |
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| Research Abstract |
Cytotoxic T lymphocyte-associated molecule-4 (CTLA-4) transduces inhibitory signals for T cell activation and regulates T cell homeostasis in vivo. Indeed, mice deficient for CTLA-4 exhibit lymphoproliferative autoimmune disease and early death at 3-4 wk of age. We show that T cells activated in the absence of IL-2/IL-2R interaction fail to express CTLA-4 on the cell surface. The lack of surface expression is due to impaired mRNA expression but not to a defect in protein trafficking. Our results demonstrate that IL-2 is essential for CTLA-4 induction in activated T cells, and suggest that the impairment of CTLA-4 induction is one of mechanisms causing fatal autoimmune disease observed in mice lacking IL-2/IL-2R system in vivo.
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