Title of article
Transforming growth factor β (TGF-β) and autoimmunity
Author/Authors
Christopher A. Aoki، نويسنده , , Andrea T. Borchers، نويسنده , , Ming Li، نويسنده , , Richard A. Flavell، نويسنده , , Christopher L. Bowlus، نويسنده , , Aftab A. Ansari، نويسنده , , M. Eric Gershwin، نويسنده ,
Issue Information
روزنامه با شماره پیاپی سال 2005
Pages
10
From page
450
To page
459
Abstract
TGF-β1 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-β receptor type II in T cells have enabled the study of cell lineage specific effects of TGF-β providing clues to the potential etiology of autoimmunity. These studies suggest that TGF-β 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
Keywords
animal models , autoimmunity , pathophysiology , TGF-h , Dominant negative TGF-h receptor type II
Journal title
Autoimmunity Reviews
Serial Year
2005
Journal title
Autoimmunity Reviews
Record number
474600
Link To Document