Th17 cells give rise to Th1 cells that are required for the pathogenesis of colitis.

摘要: Th17 cells reactive to the enteric microbiota are central pathogenesis of certain types inflammatory bowel disease. However, display substantial developmental plasticity, such that some progeny cell precursors retain a predominantly IL-17A(+) phenotype, whereas others extinguish IL-17 expression and acquire IFN-γ, giving rise "Th1-like" cells. It remains unclear what role these subsets play in Using transfer model colitis, we found IFN-γ-deficient retained an phenotype were unable induce colitis recipients. Development disease required transition subset Th1-like was contingent on both Stat4 T-bet, but not IL-12 or IFN-γ receptors. Moreover, could provide "help" for development pathogenic Th1 from naive precursors. These results indicate potent mediators by dual mechanisms: directly transitioning supporting classic