دورية أكاديمية

IRF8 deficiency induces the transcriptional, functional, and epigenetic reprogramming of cDC1 into the cDC2 lineage.

التفاصيل البيبلوغرافية
العنوان: IRF8 deficiency induces the transcriptional, functional, and epigenetic reprogramming of cDC1 into the cDC2 lineage.
المؤلفون: Lança T; Mucosal Immunology group, Department of Health Technology, Technical University of Denmark, Kemitorvet, 2800 Kgs. Lyngby, Denmark., Ungerbäck J; Division of Molecular Hematology, Lund University, 22184 Lund, Sweden., Da Silva C; Immunology Section, Department of Experimental Medicine, Lund University, BMC D14, 221-84 Lund, Sweden., Joeris T; Immunology Section, Department of Experimental Medicine, Lund University, BMC D14, 221-84 Lund, Sweden., Ahmadi F; Immunology Section, Department of Experimental Medicine, Lund University, BMC D14, 221-84 Lund, Sweden., Vandamme J; Mucosal Immunology group, Department of Health Technology, Technical University of Denmark, Kemitorvet, 2800 Kgs. Lyngby, Denmark., Svensson-Frej M; Mucosal Immunology group, Department of Health Technology, Technical University of Denmark, Kemitorvet, 2800 Kgs. Lyngby, Denmark., Mowat AM; Centre for Immunobiology, Institute of Infection, Immunity and Inflammation, College of Medicine, Veterinary Medicine and Life Sciences, University of Glasgow, Glasgow, UK., Kotarsky K; Immunology Section, Department of Experimental Medicine, Lund University, BMC D14, 221-84 Lund, Sweden., Sigvardsson M; Division of Molecular Hematology, Lund University, 22184 Lund, Sweden; Department of Physics, Chemistry and Biology, Linköping University, 581 83 Linköping, Sweden., Agace WW; Mucosal Immunology group, Department of Health Technology, Technical University of Denmark, Kemitorvet, 2800 Kgs. Lyngby, Denmark; Immunology Section, Department of Experimental Medicine, Lund University, BMC D14, 221-84 Lund, Sweden. Electronic address: wiag@dtu.dk.
المصدر: Immunity [Immunity] 2022 Aug 09; Vol. 55 (8), pp. 1431-1447.e11. Date of Electronic Publication: 2022 Jul 12.
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Cell Press Country of Publication: United States NLM ID: 9432918 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1097-4180 (Electronic) Linking ISSN: 10747613 NLM ISO Abbreviation: Immunity Subsets: MEDLINE
أسماء مطبوعة: Publication: Cambridge, MA : Cell Press
Original Publication: Cambridge, Mass. : Cell Press, c1994-
مواضيع طبية MeSH: Dendritic Cells*/metabolism , Interferon Regulatory Factors*/genetics , Interferon Regulatory Factors*/metabolism, Epigenesis, Genetic
مستخلص: Conventional dendritic cells (cDCs) consist of two major functionally and phenotypically distinct subsets, cDC1 and cDC2, whose development is dependent on distinct sets of transcription factors. Interferon regulatory factor 8 (IRF8) is required at multiple stages of cDC1 development, but its role in committed cDC1 remains unclear. Here, we used Xcr1-cre to delete Irf8 in committed cDC1 and demonstrate that Irf8 is required for maintaining the identity of cDC1. In the absence of Irf8, committed cDC1 acquired the transcriptional, functional, and chromatin accessibility properties of cDC2. This conversion was independent of Irf4 and was associated with the decreased accessibility of putative IRF8, Batf3, and composite AP-1-IRF (AICE)-binding elements, together with increased accessibility of cDC2-associated transcription-factor-binding elements. Thus, IRF8 expression by committed cDC1 is required for preventing their conversion into cDC2-like cells.
Competing Interests: Declaration of interests The authors declare no competing interests.
(Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.)
التعليقات: Comment in: Trends Immunol. 2022 Sep;43(9):687-689. (PMID: 35963772)
فهرسة مساهمة: Keywords: ATAC-sequencing; IRF; IRF4; IRF8; cDC1; cDC2; dendritic cell identity; transcription factor; transcriptional regulation; transcriptional reprogramming
المشرفين على المادة: 0 (Interferon Regulatory Factors)
تواريخ الأحداث: Date Created: 20220713 Date Completed: 20220812 Latest Revision: 20221018
رمز التحديث: 20221213
DOI: 10.1016/j.immuni.2022.06.006
PMID: 35830859
قاعدة البيانات: MEDLINE
الوصف
تدمد:1097-4180
DOI:10.1016/j.immuni.2022.06.006