An intestinal TH17 cell-derived subset can initiate cancer
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 int...
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| Veröffentlicht in: | Nature immunology 2024-07, Vol.25 (9), p.1637-1649 |
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| creator | Fesneau, Olivier Thevin, Valentin Pinet, Valérie Goldsmith, Chloe Vieille, Baptiste M’Homa Soudja, Saïdi Lattanzio, Rossano Hahne, Michael Dardalhon, Valérie Hernandez-Vargas, Hector Benech, Nicolas Marie, Julien C. |
| description | 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.
Here, the authors show that there is a pretumorigenic T
H
17 subset in the intestines that can convert to being tumorigenic under the control of KLF6 and that this process can be prevented by TGFβ1 production from intestinal epithelial cells. |
| doi_str_mv | 10.1038/s41590-024-01909-7 |
| format | Article |
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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.
Here, the authors show that there is a pretumorigenic T
H
17 subset in the intestines that can convert to being tumorigenic under the control of KLF6 and that this process can be prevented by TGFβ1 production from intestinal epithelial cells.</description><identifier>ISSN: 1529-2908</identifier><identifier>ISSN: 1529-2916</identifier><identifier>EISSN: 1529-2916</identifier><identifier>DOI: 10.1038/s41590-024-01909-7</identifier><language>eng</language><publisher>New York: Nature Publishing Group US</publisher><subject>631/250/1619/554/1898/1273 ; 631/250/256/2515 ; 631/250/580 ; Biomedical and Life Sciences ; Biomedicine ; Cancer ; Cytokines ; Epithelial cells ; Epithelium ; Growth factors ; Helper cells ; Immunology ; Infectious Diseases ; Inflammation ; Interleukin 17 ; Intestine ; Kinases ; Life Sciences ; Lymphocytes ; Lymphocytes T ; Phosphorylation ; Small intestine ; Transcription factors ; Transforming growth factor-b1 ; γ-Interferon</subject><ispartof>Nature immunology, 2024-07, Vol.25 (9), p.1637-1649</ispartof><rights>The Author(s) 2024</rights><rights>The Author(s) 2024. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2024. The Author(s).</rights><rights>Attribution</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c267t-131d22655d1163fee07c4d50f8989c646916399c015ea7fa414c6f38fdcbfc5e3</cites><orcidid>0000-0001-6045-2103 ; 0000-0002-0548-1160 ; 0000-0002-4226-0471 ; 0000-0001-9803-4476 ; 0000-0001-6713-7923 ; 0000-0002-1041-4333 ; 0000-0002-5663-0226 ; 0000-0003-0533-2920</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/s41590-024-01909-7$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/s41590-024-01909-7$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>230,314,776,780,881,27903,27904,41467,42536,51297</link.rule.ids><backlink>$$Uhttps://hal.science/hal-04675685$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Fesneau, Olivier</creatorcontrib><creatorcontrib>Thevin, Valentin</creatorcontrib><creatorcontrib>Pinet, Valérie</creatorcontrib><creatorcontrib>Goldsmith, Chloe</creatorcontrib><creatorcontrib>Vieille, Baptiste</creatorcontrib><creatorcontrib>M’Homa Soudja, Saïdi</creatorcontrib><creatorcontrib>Lattanzio, Rossano</creatorcontrib><creatorcontrib>Hahne, Michael</creatorcontrib><creatorcontrib>Dardalhon, Valérie</creatorcontrib><creatorcontrib>Hernandez-Vargas, Hector</creatorcontrib><creatorcontrib>Benech, Nicolas</creatorcontrib><creatorcontrib>Marie, Julien C.</creatorcontrib><title>An intestinal TH17 cell-derived subset can initiate cancer</title><title>Nature immunology</title><addtitle>Nat Immunol</addtitle><description>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.
Here, the authors show that there is a pretumorigenic T
H
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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.
Here, the authors show that there is a pretumorigenic T
H
17 subset in the intestines that can convert to being tumorigenic under the control of KLF6 and that this process can be prevented by TGFβ1 production from intestinal epithelial cells.</abstract><cop>New York</cop><pub>Nature Publishing Group US</pub><doi>10.1038/s41590-024-01909-7</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0001-6045-2103</orcidid><orcidid>https://orcid.org/0000-0002-0548-1160</orcidid><orcidid>https://orcid.org/0000-0002-4226-0471</orcidid><orcidid>https://orcid.org/0000-0001-9803-4476</orcidid><orcidid>https://orcid.org/0000-0001-6713-7923</orcidid><orcidid>https://orcid.org/0000-0002-1041-4333</orcidid><orcidid>https://orcid.org/0000-0002-5663-0226</orcidid><orcidid>https://orcid.org/0000-0003-0533-2920</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | 631/250/1619/554/1898/1273 631/250/256/2515 631/250/580 Biomedical and Life Sciences Biomedicine Cancer Cytokines Epithelial cells Epithelium Growth factors Helper cells Immunology Infectious Diseases Inflammation Interleukin 17 Intestine Kinases Life Sciences Lymphocytes Lymphocytes T Phosphorylation Small intestine Transcription factors Transforming growth factor-b1 γ-Interferon |
| title | An intestinal TH17 cell-derived subset can initiate cancer |
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