Histone deacetylase 1 (HDAC1): A key player of T cell-mediated arthritis.

Animals Arthritis, Rheumatoid / etiology Biomarkers Collagen / adverse effects Cytokines / metabolism Disease Models, Animal Disease Susceptibility Gene Expression Regulation Histone Deacetylase 1 / genetics Humans Inflammation Mediators / metabolism Mice Mice, Knockout T-Lymphocyte Subsets / immunology T-Lymphocytes / immunology

CCR6 HDACs Histone deacetylases Rheumatoid arthritis T cells

Journal

Journal of autoimmunity

ISSN: 1095-9157

Titre abrégé: J Autoimmun

Pays: England

ID NLM: 8812164

Informations de publication

Date de publication:
03 2020

Historique:

received: 25 06 2019

revised: 20 09 2019

accepted: 02 12 2019

pubmed: 31 12 2019

medline: 6 7 2021

entrez: 30 12 2019

Statut: ppublish

Résumé

Rheumatoid Arthritis (RA) represents a chronic T cell-mediated inflammatory autoimmune disease. Studies have shown that epigenetic mechanisms contribute to the pathogenesis of RA. Histone deacetylases (HDACs) represent one important group of epigenetic regulators. However, the role of individual HDAC members for the pathogenesis of arthritis is still unknown. In this study we demonstrate that mice with a T cell-specific deletion of HDAC1 (HDAC1-cKO) are resistant to the development of Collagen-induced arthritis (CIA), whereas the antibody response to collagen type II was undisturbed, indicating an unaltered T cell-mediated B cell activation. The inflammatory cytokines IL-17 and IL-6 were significantly decreased in sera of HDAC1-cKO mice. IL-6 treated HDAC1-deficient CD4

Identifiants

DOI: 10.1016/j.jaut.2019.102379 PMID: 31883829

pubmed: 31883829

pii: S0896-8411(19)30396-8

doi: 10.1016/j.jaut.2019.102379

pii:

doi:

Substances chimiques

Biomarkers 0

Cytokines 0

Inflammation Mediators 0

Collagen 9007-34-5

Histone Deacetylase 1 EC 3.5.1.98

Types de publication

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

Langues

eng

Sous-ensembles de citation

Pagination

102379

Subventions

Organisme : Austrian Science Fund FWF

ID : P 28705

Pays : Austria

Informations de copyright

Déclaration de conflit d'intérêts

Declaration of competing interest None. This research has received support from the Innovative Medicines Initiative (IMI) Joint Undertaking under grant agreement n°115142 (BTCure), and grant agreement n(o)777357 (RTCure) resources of which are composed of financial contribution from the European Union's Framework Programmes and EFPIA companies' in kind contribution. The work has been supported by the Austrian Science Fund (FWF) project F26193 (to WE) and the FWF special research program SFB F70 (subproject F7003 to MB, F7004 to NB and F7005 to WE).