While Tregs are immunosuppressive at sites of inflammation, Tregs may express transcription factors and cytokines that parallel those of Tconv cells. Thus, Tregs express T-bet and IRF4 at sites of Th1 and Th2 inflammation, respectively [5] [6] [7] . Additionally, we and others have shown that Foxp3 + Tregs express IFN-c during infections [5, 8] . Unfractionated populations of Tregs harvested from inflammatory sites, which include cells expressing IFN-c, remain immunosuppressive. Suppression can be demonstrated in T cell proliferation assays after stimulation with either anti-CD3 mAb or virus-specific peptides [8] . In contrast, other studies suggest that a pro-inflammatory milieu may result in diminished Treg suppressive function [9] [10] [11] . In a model of experimental autoimmune encephalomyelitis (EAE), CNS-derived epitope MOG -specific Tregs showed reduced ability to inhibit proliferation of Tconv of the same specificity isolated from the inflamed CNS [9] . This reduction in inhibitory function was IL-6 and TNF-dependent.