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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

Artikel i vetenskaplig tidskrift
Författare M. Yang
K. Klocke
C. M. Hernandez
B. Z. Xu
Inger Gjertsson
K. Wing
R. Holmdahl
Publicerad i Immunology
Volym 155
Nummer/häfte 4
Sidor 446-457
ISSN 0019-2805
Publiceringsår 2018
Publicerad vid Institutionen för medicin, avdelningen för reumatologi och inflammationsforskning
Sidor 446-457
Språk en
Länkar dx.doi.org/10.1111/imm.12983
Ämnesord 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
Ämneskategorier Klinisk immunologi

Sammanfattning

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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