| Project/Area Number |
20591193
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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 |
膠原病・アレルギー・感染症内科学
|
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| Research Institution | Saitama Medical University |
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Principal Investigator |
TAKEUCHI Tsutomu Saitama Medical University, 医学部, 教授 (50179610)
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| Co-Investigator(Renkei-kenkyūsha) |
KAMEDA Hideto 慶應義塾大学, 医学部, 講師 (00265795)
YOSHIMOTO Keiko 慶應義塾大学, 医学部, 研究員 (20383292)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2010: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2009: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2008: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 自己免疫 / 上皮障害 / カドヘリン / インテグリン / CD103 / シグナル伝達 / CDIO3 |
|---|
| Research Abstract |
Given the evidence that αEβ7(CD03) expressed on T cells is involved in adhesion with E-cadherin on epithelial cells, the CD103 molecule may play a wide variety role in cellular function. In this study, it has been shown that for induction of CD103, not only the expression of TGF-βreceptor by lectin, but also signal transduction through Smad 2/3 is required. After expression of CD103, T cells become proliferate poor, and exhibit unique cytokine prolife. Since CD103+subset of cells can mediate immune-regulatory and immune- inflammatory function, farther investigation may be regained to dissect thesignal leady to two distinct function.
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