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

2015; National Academy of Sciences; Volume: 112; Issue: 22 Linguagem: Inglês

10.1073/pnas.1415675112

1091-6490

Stacey N. Harbour, Craig L. Maynard, Carlene L. Zindl, Trenton R. Schoeb, Casey T. Weaver,

Psoriasis: Treatment and Pathogenesis

Significance The Th17 subset of CD4 + T cells are important in the pathogenesis of inflammatory bowel disease (IBD), but the mechanisms of their actions, particularly the role of the development of IFN-γ–producing progeny of Th17 cells (Th1-like cells), are incompletely understood. Here, we show in a mouse model of Th17-driven IBD that transition of Th17 precursors to Th1-like cells is absolutely required for disease, because Th17 cells deficient in IFN-γ fail to induce intestinal inflammation. This transition is dependent on the transcription factors T-bet and, to a lesser extent, Stat4. These findings are relevant for clinical strategies that target IBD and suggest that focusing on both the Th17 and Th1-like arms of disease may be beneficial in therapy design.