Bcl6 is a subset-defining transcription factor of lymphoid tissue inducer-like ILC3.

Autor:	Tachó-Piñot R; Lydia Becker Institute of Immunology and Inflammation, University of Manchester, Manchester M13 9PL, UK; Division of Immunology, Immunity to Infection and Respiratory Medicine, School of Biological Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester M13 9PL, UK., Stamper CT; Center for Infectious Medicine, Department of Medicine Huddinge, Karolinska Institutet, Stockholm, Sweden; Medical Unit for Lung and Allergy Diseases, Karolinska University Hospital, Stockholm, Sweden., King JI; Lydia Becker Institute of Immunology and Inflammation, University of Manchester, Manchester M13 9PL, UK; Division of Immunology, Immunity to Infection and Respiratory Medicine, School of Biological Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester M13 9PL, UK., Matei-Rascu V; Institute of Immunology and Immunotherapy, College of Medical and Dental Sciences, University of Birmingham, Birmingham B15 2TT, UK., Richardson E; Institute of Immunology and Immunotherapy, College of Medical and Dental Sciences, University of Birmingham, Birmingham B15 2TT, UK., Li Z; Institute of Immunology and Immunotherapy, College of Medical and Dental Sciences, University of Birmingham, Birmingham B15 2TT, UK., Roberts LB; Lydia Becker Institute of Immunology and Inflammation, University of Manchester, Manchester M13 9PL, UK; Division of Immunology, Immunity to Infection and Respiratory Medicine, School of Biological Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester M13 9PL, UK., Bassett JW; Center for Infectious Medicine, Department of Medicine Huddinge, Karolinska Institutet, Stockholm, Sweden; Medical Unit for Lung and Allergy Diseases, Karolinska University Hospital, Stockholm, Sweden., Melo-Gonzalez F; Lydia Becker Institute of Immunology and Inflammation, University of Manchester, Manchester M13 9PL, UK; Division of Immunology, Immunity to Infection and Respiratory Medicine, School of Biological Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester M13 9PL, UK., Fiancette R; Institute of Immunology and Immunotherapy, College of Medical and Dental Sciences, University of Birmingham, Birmingham B15 2TT, UK., Lin IH; Bioinformatics Core Facility, University of Manchester, Manchester M13 9PL, UK., Dent A; Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN, USA., Harada Y; Laboratory of Pharmaceutical Immunology, Faculty of Pharmaceutical Sciences, Tokyo University of Science, 2641 Yamazaki, Noda, Chiba 278-8510, Japan., Finlay C; Lydia Becker Institute of Immunology and Inflammation, University of Manchester, Manchester M13 9PL, UK; Division of Immunology, Immunity to Infection and Respiratory Medicine, School of Biological Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester M13 9PL, UK; School of Medicine, Trinity Translational Medicine Institute, Trinity College Dublin, Dublin, Ireland., Mjösberg J; Center for Infectious Medicine, Department of Medicine Huddinge, Karolinska Institutet, Stockholm, Sweden; Medical Unit for Lung and Allergy Diseases, Karolinska University Hospital, Stockholm, Sweden., Withers DR; Institute of Immunology and Immunotherapy, College of Medical and Dental Sciences, University of Birmingham, Birmingham B15 2TT, UK., Hepworth MR; Lydia Becker Institute of Immunology and Inflammation, University of Manchester, Manchester M13 9PL, UK; Division of Immunology, Immunity to Infection and Respiratory Medicine, School of Biological Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester M13 9PL, UK. Electronic address: matthew.hepworth@manchester.ac.uk.
Jazyk:	angličtina
Zdroj:	Cell reports [Cell Rep] 2023 Nov 28; Vol. 42 (11), pp. 113425. Date of Electronic Publication: 2023 Nov 10.
DOI:	10.1016/j.celrep.2023.113425
Abstrakt:	Innate lymphoid cells (ILCs) are tissue-resident effector cells with roles in tissue homeostasis, protective immunity, and inflammatory disease. Group 3 ILCs (ILC3s) are classically defined by the master transcription factor RORγt. However, ILC3 can be further subdivided into subsets that share type 3 effector modules that exhibit significant ontological, transcriptional, phenotypic, and functional heterogeneity. Notably lymphoid tissue inducer (LTi)-like ILC3s mediate effector functions not typically associated with other RORγt-expressing lymphocytes, suggesting that additional transcription factors contribute to dictate ILC3 subset phenotypes. Here, we identify Bcl6 as a subset-defining transcription factor of LTi-like ILC3s in mice and humans. Deletion of Bcl6 results in dysregulation of the LTi-like ILC3 transcriptional program and markedly enhances expression of interleukin-17A (IL-17A) and IL-17F in LTi-like ILC3s in a manner in part dependent upon the commensal microbiota-and associated with worsened inflammation in a model of colitis. Together, these findings redefine our understanding of ILC3 subset biology. Competing Interests: Declaration of interests The authors declare no competing interests. (Copyright © 2023 The Author(s). Published by Elsevier Inc. All rights reserved.)
Databáze:	MEDLINE
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