An intestinal TH17 cell-derived subset can initiate cancer

Olivier Fesneau; Valentin Thevin; Valerie Pinet; Chloe Goldsmith; Baptiste Vieille; Saidi M'Homa Soudja; Rossano Lattanzio; Michael Hahne; Valerie Dardalhon; Hector Hernandez-Vargas; Nicolas Benech; Julien C. Marie

doi:10.1038/s41590-024-01909-7

An intestinal TH17 cell-derived subset can initiate cancer

Olivier Fesneau, Valentin Thevin, Valerie Pinet, Chloe Goldsmith, Baptiste Vieille, Saidi M'Homa Soudja, Rossano Lattanzio, Michael Hahne, Valerie Dardalhon, Hector Hernandez-Vargas, Nicolas Benech, Julien C. Marie

Western Sydney University

Claude Bernard Lyon 1 University

Research output: Contribution to journal › Article › peer-review

4 Citations (Scopus)

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 (TH17) 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-Î³. The development of this cell type is inhibited by transforming growth factor-Î²1 (TGFÎ²1) produced by intestinal epithelial cells. TGFÎ² signaling acts on the pretumorigenic TH17 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.

Original language	English
Pages (from-to)	1637-1649
Number of pages	13
Journal	Nature Immunology
Volume	25
Issue number	9
DOIs	https://doi.org/10.1038/s41590-024-01909-7
Publication status	Published - Sept 2024

Bibliographical note

Publisher Copyright:
© The Author(s) 2024.

Open Access - Access Right Statement

This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the articles Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article�s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.1038/s41590-024-01909-7

Cite this

@article{e5772fceab45454f826430d17235b149,

title = "An intestinal TH17 cell-derived subset can initiate cancer",

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 (TH17) 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-{\^I}³. The development of this cell type is inhibited by transforming growth factor-{\^I}²1 (TGF{\^I}²1) produced by intestinal epithelial cells. TGF{\^I}² signaling acts on the pretumorigenic TH17 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.",

author = "Olivier Fesneau and Valentin Thevin and Valerie Pinet and Chloe Goldsmith and Baptiste Vieille and Soudja, {Saidi M'Homa} and Rossano Lattanzio and Michael Hahne and Valerie Dardalhon and Hector Hernandez-Vargas and Nicolas Benech and Marie, {Julien C.}",

note = "Publisher Copyright: {\textcopyright} The Author(s) 2024.",

year = "2024",

month = sep,

doi = "10.1038/s41590-024-01909-7",

language = "English",

volume = "25",

pages = "1637--1649",

journal = "Nature Immunology",

issn = "1529-2908",

publisher = "Nature Publishing Group",

number = "9",

}

TY - JOUR

T1 - An intestinal TH17 cell-derived subset can initiate cancer

AU - Fesneau, Olivier

AU - Thevin, Valentin

AU - Pinet, Valerie

AU - Goldsmith, Chloe

AU - Vieille, Baptiste

AU - Soudja, Saidi M'Homa

AU - Lattanzio, Rossano

AU - Hahne, Michael

AU - Dardalhon, Valerie

AU - Hernandez-Vargas, Hector

AU - Benech, Nicolas

AU - Marie, Julien C.

PY - 2024/9

Y1 - 2024/9

N2 - 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 (TH17) 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-Î³. The development of this cell type is inhibited by transforming growth factor-Î²1 (TGFÎ²1) produced by intestinal epithelial cells. TGFÎ² signaling acts on the pretumorigenic TH17 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.

AB - 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 (TH17) 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-Î³. The development of this cell type is inhibited by transforming growth factor-Î²1 (TGFÎ²1) produced by intestinal epithelial cells. TGFÎ² signaling acts on the pretumorigenic TH17 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.

UR - https://hdl.handle.net/1959.7/uws:78117

UR - http://www.scopus.com/inward/record.url?scp=85199705595&partnerID=8YFLogxK

U2 - 10.1038/s41590-024-01909-7

DO - 10.1038/s41590-024-01909-7

M3 - Article

SN - 1529-2908

VL - 25

SP - 1637

EP - 1649

JO - Nature Immunology

JF - Nature Immunology

IS - 9

ER -

An intestinal TH17 cell-derived subset can initiate cancer

Abstract

Bibliographical note

Open Access - Access Right Statement

UN SDGs

Access to Document

Other files and links

Fingerprint

Cite this