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Regulatory T cells control epitope spreading in autoimmune arthritis independent of cytotoxic T-lymphocyte antigen-4 VOL EA, 1995, IMMUNITY, V3, P541

Journal article
Authors M. Yang
K. Klocke
C. M. Hernandez
B. Z. Xu
Inger Gjertsson
K. Wing
R. Holmdahl
Published in Immunology
Volume 155
Issue 4
Pages 446-457
ISSN 0019-2805
Publication year 2018
Published at Institute of Medicine, Department of Rheumatology and Inflammation Research
Pages 446-457
Language en
Links dx.doi.org/10.1111/imm.12983
Keywords autoimmune arthritis, cytotoxic T-lymphocyte antigen-4, epitope spreading, regulatory T cells, rheumatoid-arthritis, chronic inflammation, tissue attack, tnf-alpha, ctla-4, mice, disease, mechanisms, tolerance, adulthood, Immunology
Subject categories Clinical immunology

Abstract

CD4(+) Foxp3(+) regulatory T (Treg) cells can control both cellular and humoral immune responses; however, when and how Treg cells play a predominant role in regulating autoimmune disease remains elusive. To deplete Treg cells in vivo at given time-points, we used a mouse strain, susceptible to glucose-6-phosphate isomerase peptide-induced arthritis (GIA), in which the deletion of Treg cells can be controlled by diphtheria toxin treatment. By depleting Treg cells in the GIA mouse model, we found that a temporary lack of Treg cells at both priming and onset exaggerated disease development. Ablation of Treg cells led to the expansion of antigen-specific CD4(+) T cells including granulocyte-macrophage colony-stimulating factor, interferon-gamma and interleukin-17-producing T cells, and promoted both T-cell and B-cell epitope spreading, which perpetuated arthritis. Interestingly, specific depletion of cytotoxic T-lymphocyte antigen-4 (CTLA-4) on Treg cells only, was sufficient to protect mice from GIA, due to the expansion of CTLA-4(-) Treg cells expressing alternative suppressive molecules. Collectively, our findings suggest that Treg cells, independently of CTLA-4, act as the key driving force in controlling autoimmune arthritis development.

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