Transforming growth factor β (TGF-β) and autoimmunity

被引：107

作者：

Aoki, CA

Borchers, AT

Li, M

Flavell, RA

Bowlus, CL

Ansari, AA

Gershwin, ME

机构：

[1] Univ Calif Davis, Sch Med, Div Rheumatol Allergy & Clin Immunol, Davis, CA 95616 USA

[2] Yale Univ, Sch Med, Howard Hughes Med Inst, New Haven, CT 06520 USA

[3] Univ Calif Davis, Dept Internal Med, Div Gastroenterol, Davis, CA 95616 USA

[4] Emory Univ, Sch Med, Dept Pathol, Atlanta, GA 30322 USA

来源：

AUTOIMMUNITY REVIEWS | 2005年 / 4卷 / 07期

关键词：

TGF-beta; autoimmunity; animal models; dominant negative TGF-beta receptor type II; pathophysiology;

D O I：

10.1016/j.autrev.2005.03.006

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

TGF-beta 1 deficient mice develop multifocal inflammatory autoimmune disease and serve as a valuable animal model of autoimmunity. Transgenic expression of a dominant negative form of TGF-beta receptor type II in T cells have enabled the study of cell lineage specific effects of TGF-beta providing clues to the potential etiology of autoimmunity. These studies suggest that TGF-beta deficiency may induce autoimmune disease by influencing a number of immunological phenomena including lymphocyte activation and differentiation, cell adhesion molecule expression, regulatory T cell function, the expression of MHC molecules and cytokines, and cell apoptosis. The spectrum of effects appears to be significant in mucosal immunity and may contribute to the pathogenesis of inflammatory bowel disease. (c) 2005 Elsevier B.V. All rights reserved.

引用

页码：450 / 459

页数：10

共 40 条

[1] TGF-β-dependent mechanisms mediate restoration of self-tolerance induced by antibodies to CD3 in overt autoimmune diabetes [J].