Abstract

The regulatory T cells (Treg) restrain immune responses through elaboration of suppressor function dependent upon expression of the transcription factor Foxp3. Despite a critical role for Treg cells in maintaining lympho-myeloid homeostasis, it remains unclear whether a single mechanism or multiple mechanisms of Treg-mediated suppression are operating in vivo, and how redundant such mechanisms might be. We address these questions using a genetic approach. Our studies suggest that Treg cells utilize multiple means to limit immune response. Furthermore, these mechanisms are likely non-redundant with a distinct suppressor mechanism playing a prominent and identifiable role at a particular tissue and inflammatory setting.