The AP1 Transcription Factor Fosl2 Promotes Systemic Autoimmunity and Inflammation by Repressing Treg Development.


Journal

Cell reports
ISSN: 2211-1247
Titre abrégé: Cell Rep
Pays: United States
ID NLM: 101573691

Informations de publication

Date de publication:
30 06 2020
Historique:
received: 14 10 2019
revised: 27 03 2020
accepted: 05 06 2020
entrez: 2 7 2020
pubmed: 2 7 2020
medline: 29 4 2021
Statut: ppublish

Résumé

Regulatory T cells (Tregs) represent a major population in the control of immune homeostasis and autoimmunity. Here we show that Fos-like 2 (Fosl2), a TCR-induced AP1 transcription factor, represses Treg development and controls autoimmunity. Mice overexpressing Fosl2 (Fosl2

Identifiants

pubmed: 32610127
pii: S2211-1247(20)30807-X
doi: 10.1016/j.celrep.2020.107826
pii:
doi:

Substances chimiques

DNA-Binding Proteins 0
Forkhead Transcription Factors 0
Fos-Related Antigen-2 0
Fosl2 protein, mouse 0
Foxp3 protein, mouse 0
Rag2 protein, mouse 0
Receptors, Antigen, T-Cell 0
Transcription Factor AP-1 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

107826

Informations de copyright

Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Interests O.D. had consultancy relationships and/or has received research funding from A. Menarini, Acceleron Pharma, Amgen, AnaMar, Bayer, Boehringer Ingelheim, Catenion, CSL Behring, ChemomAb, Ergonex, GSK, Inventiva, Italfarmaco, iQone, iQvia, Lilly, medac, Medscape, Mitsubishi Tanabe Pharma, Merck Sharpe & Dohme (MSD), Novartis, Pfizer, Roche, Sanofi, Blade Therapeutics, CSL Behrings Target Bio Science, and UCB in the area of potential treatments for scleroderma and its complications. In addition, Prof. Distler has a patent mir-29 for the treatment of systemic sclerosis (US8247389, EP2331143). R.H. and A.S. are full-time employees of Sanofi-Genzyme.

Auteurs

Florian Renoux (F)

Center of Experimental Rheumatology, Department of Rheumatology, University Hospital Zurich, Zurich, Switzerland.

Mara Stellato (M)

Center of Experimental Rheumatology, Department of Rheumatology, University Hospital Zurich, Zurich, Switzerland.

Claudia Haftmann (C)

Institute of Experimental Immunology, University of Zurich, Zurich, Switzerland.

Alexander Vogetseder (A)

Department of Pathology, Luzerner Kantonspital, Lucerne, Switzerland.

Riyun Huang (R)

Sanofi, Immunology and Inflammation Research TA, Cambridge, MA 02139, USA.

Arun Subramaniam (A)

Sanofi, Immunology and Inflammation Research TA, Cambridge, MA 02139, USA.

Mike O Becker (MO)

Center of Experimental Rheumatology, Department of Rheumatology, University Hospital Zurich, Zurich, Switzerland.

Przemyslaw Blyszczuk (P)

Center of Experimental Rheumatology, Department of Rheumatology, University Hospital Zurich, Zurich, Switzerland; Department of Clinical Immunology, Jagiellonian University Medical College, Cracow, Poland.

Burkhard Becher (B)

Institute of Experimental Immunology, University of Zurich, Zurich, Switzerland.

Jörg H W Distler (JHW)

Department of Internal Medicine 3, University of Erlangen-Nuremberg, Erlangen, Germany.

Gabriela Kania (G)

Center of Experimental Rheumatology, Department of Rheumatology, University Hospital Zurich, Zurich, Switzerland.

Onur Boyman (O)

Department of Immunology, University Hospital Zurich, Zurich, Switzerland; Faculty of Medicine, University of Zurich, Zurich, Switzerland.

Oliver Distler (O)

Center of Experimental Rheumatology, Department of Rheumatology, University Hospital Zurich, Zurich, Switzerland; Faculty of Medicine, University of Zurich, Zurich, Switzerland. Electronic address: oliver.distler@usz.ch.

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Classifications MeSH