These results clearly support the idea that leptin is mediating a shift from Th2 to Th1 response in L. donovani–infected normal mice, as was observed in infections with other pathogenic agents.47,63 Furthermore, our results showed that CD4+ and CD8+ T-cell impairment associated with VL could be rescued by leptin treatment as indicated by the increased percentage of Leishmania Ag–specific IFNγ and significantly increased IFNγ/IL10 ratio in both CD4+ and CD8+ T cells. Here, LEP is linked to infection.