2010 Fiscal Year Final Research Report
Analysis on signal transduction pathway through CD103 molecule
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 |
Section | 一般 |
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 |
Principal Investigator |
TAKEUCHI Tsutomu Saitama Medical University, 医学部, 教授 (50179610)
|
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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Keywords | 自己免疫 / 上皮障害 / カドヘリン / インテグリン / CD103 |
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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