Transforming growth factor β (TGF-β) and autoimmunity

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.