Chronic antigenic stimulation is known to cause T cell functional exhaustion and death. During Mtb infections, antigen specific CD4 T cells are subject to chronic antigenic stimulation but a sizeable population of these cells survives and maintains the ability to produce IFN-γ. How these cells are maintained is not yet understood. Mtb-specific CD4 T cells can be classified based on the surface expression of the inhibitory receptors PD1 and KLRG1. The PD1+ cells proliferate robustly but produce low amounts of IFN-γ while KLRG1+ cells proliferate less but produce large amounts of IFN-γ. Significantly, the PD1+ cells are capable of differentiating into KLRG1+ cells and not vice versa indicating that a self-renewing progenitor population may be contained within the PD1+ cells. On further characterization we have found that PD1+ cells are heterogeneous containing three different subsets based on expression of the chemokine receptor CXCR5 i.e. PD1+CXCR5hi cells that resemble Tfh cells, PD1+CXCR5int and PD1+CXCR5lo cells. We found that B cells were not required to maintain the Tfh like cells or overall Mtb-specific CD4 T cells. However, using mixed bone marrow chimeras we found that intrinsic CXCR5 expression on CD4 T cells is required to maintain Mtb-specific CD4 T cells. Taken together, these studies indicate that during Mtb infections, a subset of CD4 T cells capable of self-renewal is induced and intrinsic CXCR5 is important for its maintenance.