Adding to this complexity, under experimental infectious challenges, DHEA appears to stimulate IFN-γ in parasitic infections, thereby promoting response (253) in a striking similarity to estrogen’s impact on IFN-γ (254), and also, it improves macrophage phagocytosis via NO upregulation in bacterial challenge through favoring of Th1 responses in contrast to Th2 (increased IL-2 and IFN-α; decreased IL-4 and IL-10) (255). Here, IFNG is linked to parasitic infectious disease.