Transforming growth factor beta (TGF-beta) and autoimmunity

Abstract

TGF-beta1 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.