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            <funder>This work was supported by grants from INSERM Single Cell Plan Cancer Program (J.C.M. and H.H.-V.), LabEx DEVweCAN ANR investissement d’Avenir ANR-10-LABX-61 (J.C.M.), the Labelisation Ligue Nationale Contre Cancer (EL-2016 and EL-2021; J.C.M.), PLASCAN program (H.H.-V.), LYRICAN INCa-DGOS-Inserm_12563 and LYIRICAN+ INCa-DGOS-INSERM-ITMO cancer_18003 (J.C.M.) and the Labelisation Fondation pour la Recherche Medicale (V.P. and M.H.). O.F. and V.T. were supported by both the French ministry of research fellowship and the Ligue Nationale Contre Cancer. C.G. was supported by the ERICAN program.</funder>
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                <title level="j">Nature Immunology</title>
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              <p>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.</p>
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