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An intestinal TH17 cell-derived subset can initiate cancer

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Fesneau, Olivier | Thevin, Valentin | Pinet, Valérie | Goldsmith, Chloe | Vieille, Baptiste | Soudja, Saidi | Lattanzio, Rossano | Hahne, Michael | Dardalhon, Valérie | Hernandez-Vargas, Hector | Benech, Nicolas | Marie, Julien

Edité par CCSD ; Nature Publishing Group -

International audience. Abstract Approximately 25% of cancers are preceded by chronic inflammation that occurs at the site of tumor development. However, whether this multifactorial oncogenic process, which commonly occurs in the intestines, can be initiated by a specific immune cell population is unclear. Here, we show that an intestinal T cell subset, derived from interleukin-17 (IL-17)-producing helper T (T H 17) cells, induces the spontaneous transformation of the intestinal epithelium. This subset produces inflammatory cytokines, and its tumorigenic potential is not dependent on IL-17 production but on the transcription factors KLF6 and T-BET and interferon-γ. The development of this cell type is inhibited by transforming growth factor-β1 (TGFβ1) produced by intestinal epithelial cells. TGFβ signaling acts on the pretumorigenic T H 17 cell subset, preventing its progression to the tumorigenic stage by inhibiting KLF6-dependent T-BET expression. This study therefore identifies an intestinal T cell subset initiating cancer.

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