Another consequence of IL-12 treatment is the induction of IFN-c expression by Tregs. Tregs express IFN-c at sites of inflammation under conditions of Th1-type lethal and non-lethal infections [5, 8] . It has been difficult to determine whether IFN-c affects Treg suppressive function, since Tregs in these settings include both IFN-c + and IFN-ccells. Here we showed that IFN-c expression did not diminish Treg suppressive function. These results are in agreement with others showing that in vitro-generated IFN-c + and IFN-c -Tregs were equally suppressive in a mouse model of colitis [13] . In other experimental settings, loss of Foxp3 and gain of inflammatory cytokine expression suggested that Tregs converted into effector T cells [22, 47] . If Tregs at sites of inflammation can generally express IFN-c and still remain suppressive, these results raise the possibility that IFN-c + Tregs, instead of entering the effector T cell pool, could lose IFN-c and revert to a classic Treg phenotype. Whether these cells would preferentially re-express IFN-c on repeat exposure to antigen remains to be determined.