@article{9cded38c8432483d832a501b2dc02d8a,
title = "Campylobacter infection promotes IFNγ-dependent intestinal pathology via ILC3 to ILC1 conversion",
abstract = "Innate lymphoid cells (ILCs) are a heterogeneous family of immune regulators that protect against mucosal pathogens but can also promote intestinal pathology. Although the plasticity between ILCs populations has been described, the role of mucosal pathogens in inducing ILC conversion leading to intestinal pathology remains unclear. Here we demonstrate that IFNγ-producing ILCs are responsible for promoting intestinal pathology in a mouse model of enterocolitis caused by Campylobacter jejuni, a common human enteric pathogen. Phenotypic analysis revealed a distinct population of IFNγ-producing NK1.1−T-bet+ILCs that accumulated in the intestine of C. jejuni-infected mice. Adoptive transfer experiments demonstrated their capacity to promote intestinal pathology. Inactivation of T-bet in NKp46+ ILCs ameliorated disease. Transcriptome analysis and cell-fate mapping experiments revealed that IFNγ-producing NK1.1−ILCs correspond to ILC1 profile and develop from RORγt+ progenitors. Collectively, we identified a distinct population of NK1.1−ex-ILC3s that promotes intestinal pathology through IFNγ production in response to C. jejuni infection.",
author = "Muraoka, {Wayne T.} and Korchagina, {Anna A.} and Qingqing Xia and Shein, {Sergey A.} and Xi Jing and Zhao Lai and Weldon, {Korri S.} and Wang, {Li Ju} and Yidong Chen and Kummer, {Lawrence W.} and Markus Mohrs and Eric Vivier and Koroleva, {Ekaterina P.} and Tumanov, {Alexei V.}",
note = "Funding Information: This research was supported by grants from NIH (AI135574, AI111000), Pfizer (WI215053), and Trudeau Institute. WTM was supported by USDA NIFA (2014-67012-22276). AVT was supported by the Crohn{\textquoteright}s and Colitis Foundation (SRA#294083), the Max and Minnie Tomerlin Voelcker Fund, and by the William and Ella Owens Medical Research Foundation. We thank Dr. Joseph Sun (MSKCC) for providing NKp46-Cre mice. Genome Sequencing Facility at the Greehey Children{\textquoteright}s Cancer Research Institute is supported with funding from NIH (NCI P30 CA54174, CTSA 1UL1 RR025767-01, and 1S10 OD021805-01), and from Cancer Prevention and Research Institute of Texas (RP160732) with support to YC, and ZL. The E.V. laboratory at CIML and Assistance-Publique des H{\^o}pitaux de Marseille is supported by funding from the European Research Council (ERC) under the European Union's Horizon 2020 research and innovation program (TILC, grant agreement No. 694502), the Agence Nationale de la Recherche including the PIONEER Project (ANR-17-RHUS-0007), MSDAvenir, Innate Pharma and institutional grants to the CIML (INSERM, CNRS, and Aix-Marseille University) and to Marseille Immunopole. Data was generated in the Flow Cytometry Shared Resource Facility which is supported by UT Health San Antonio, NIH-NCI P30 CA054174-20 (CTRC at UTHSCSA) and UL1 TR001120 (CTSA grant). Publisher Copyright: {\textcopyright} 2020, Society for Mucosal Immunology.",
year = "2021",
month = may,
doi = "10.1038/s41385-020-00353-8",
language = "English (US)",
volume = "14",
pages = "703--716",
journal = "Mucosal Immunology",
issn = "1933-0219",
publisher = "Nature Publishing Group",
number = "3",
}