IL17A and Alzheimer disease: Furthermore, as splenic CD4+ T cells from IL-7 KO mice are defective in producing IFN-γ and IL-17 rather than Th2-type cytokines (e.g., IL-4 or IL-5), the decrease of IFN-γ and IL-17 production may trigger the initiation of Th2 immune responses, consequently leading to accelerated AD development in IL-7 KO mice (Figure S2).