This profound suppression in Mtb-specific and maximum IFN-γ production by T cells in helminth positive individuals may be due to the expansion of Mtb-specific memory cells primed to produce Th-2 type cytokines [30], or CD4+ T cell-related epigenetic changes induced by helminth infection as previously described for Schistosomiasis and Ascaris infection in recently TB-exposed children where CD4+ T cell DNA hypermethylation resulted in decreased TB-specific IFN-γ and TNF expression [31]. This evidence concerns the gene CD4 and tuberculosis.