Infection with the intracellular protozoan parasite Leishmania major induces a state of concomitant immunity wherein secondary immunity is dependent upon the persistence of the original pathogen. Our laboratory has described two populations of Leishmania-induced CD4+ T cells that contribute to immunity: CD62L high central memory T (T CM) cells and CD62L low effector T cells. To determine whether the prosurvival cytokine IL-7 contributes to maintaining these T cells, we examined expression of the IL7R on CD4+ T cells activated during L. major infection. We found that T CM cells present in chronically infected mice expressed high levels of the IL7R. However, in addition to the expression of the IL7R by T CM cells, CD62L low cells responding to L. major infection expressed the IL7R. Additional experiments revealed that a large percentage of the IL7R high CD62L low cells were Th1 cells, based on transcription at the IFN-γ locus and up-regulation of the Th1-promoting transcription factor T-bet. The up-regulation of T-bet did not prevent IL7R expression by L. major-responding CD4+ T cells, nor did the absence of T-bet result in increased IL7R expression. Finally, blockade of IL7R signaling decreased the number of T-bet+ CD4+ T cells, reduced IFN-γ production, and inhibited delayed-type hypersensitivity responses in immune mice challenged with L. major, indicating that IL7R signaling contributes to the maintenance of Th1 effector cells. Thus, both T CM and Th1 effector cells can express the IL7R during chronic L. major infection, which provides a potential means for their long-term survival in addition to the presence of persisting parasites.