Resistance to infection is conferred by development of effective T helper cell 1-type (Th1) responses, mounted upon release of a pleiotropic interleukin (IL)-12 and interferon (IFN)-γ cytokine network, and boosted by pro-inflammatory (tumor necrosis factor (TNF), IL-23, IL-17A) and Th2-promoting (IL-4) mediators [13-17]. This evidence concerns the gene IL17A and infection.