TGF-b Directly Targets Effector T Cells

healthy individuals (Danke et al., 2004). Importantly, these auto- diators of the disease because depletion of CD4+ or CD8+ T cellsreactive T cells are normally prevented from inducing autoim-mune diseases. In addition, regulatory mechanisms are in place to prevent collateral tissue damage as a result of exuberant T cell responses to pathogens or innocuous environmental entities such as the commensal flora. How self-inflicted inflammation is controlled in the steady state and during infection is a topic of active research. Previous studies with animal models have established essential functions for the cytokines transforming growth factor-b (TGF-b) and inerleukin-10 (IL-10) in inhibiting T cell-mediated immunopathology (Li et al., 2006b; Moore et al., 2001). In this review, we will discuss recent insights gained in the understanding of the mechanisms by which TGF-b and IL-10 regulate inflammatory T cell responses