TGF-β, T-cell tolerance and anti-CD3 therapy

被引：20

作者：

Bommireddy, R ^{[1
]}

Doetschman, T ^{[1
]}

机构：

[1] Univ Cincinnati, Coll Med, Dept Mol Genet Biochem & Microbiol, Cincinnati, OH 45267 USA

来源：

TRENDS IN MOLECULAR MEDICINE | 2004年 / 10卷 / 01期

关键词：

D O I：

10.1016/j.molmed.2003.11.007

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Recent studies by Chatenoud and co-workers suggest that non-mitogenic F(ab')(2) fragments of anti-CD3 antibodies, which cannot bind the Fc receptor, induce a prolonged period of tolerance and prevent diabetes in nonobese diabetic (NOD) mice. Tolerance is established by regulatory T cells through the production of transforming growth factor-beta1 (TGF-betal), but the mechanism by which TGF-beta1 confers this activity is unclear. Analysis of mice deficient in TGF-beta1 suggests that TGF-beta1 raises the threshold at which intracellular calcium activates T cells to a level that prevents an autoimmune response.

引用

页码：3 / 9

页数：7

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