It has been postulated that the antigen-specific immunosuppression observed in disseminated CL and the resulting clinical syndrome could partially be due to the ability of the infecting parasite to induce a predominance of IL-10 over IFN-γ.[87] This Th2 mechanism inhibits macrophage activation, thereby permitting intracellular replication of the parasite.[85] HIV plays an important role in induction of a Th2-like state, along with CD4+ T cell depletion, ultimately inhibiting the Th1-type cytokine secretion and increasing susceptibility to infection.[85]. This evidence concerns the gene IFNG and infection.