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Regulatory T cells ...
Regulatory T cells control epitope spreading in autoimmune arthritis independent of cytotoxic T-lymphocyte antigen-4 VOL EA, 1995, IMMUNITY, V3, P541
- Artikel/kapitelEngelska2018
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LIBRIS-ID:oai:gup.ub.gu.se/274328
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https://gup.ub.gu.se/publication/274328URI
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https://doi.org/10.1111/imm.12983DOI
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http://kipublications.ki.se/Default.aspx?queryparsed=id:139552828URI
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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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Klocke, K.Karolinska Institutet
(författare)
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Hernandez, C. M.
(författare)
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Xu, B. Z.Karolinska Institutet
(författare)
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Gjertsson, Inger,1962Gothenburg University,Göteborgs universitet,Institutionen för medicin, avdelningen för reumatologi och inflammationsforskning,Institute of Medicine, Department of Rheumatology and Inflammation Research(Swepub:gu)xgjein
(författare)
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Wing, K.
(författare)
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Holmdahl, R.Karolinska Institutet
(författare)
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Karolinska InstitutetInstitutionen för medicin, avdelningen för reumatologi och inflammationsforskning
(creator_code:org_t)
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Ingår i:Immunology: Wiley155:4, s. 446-4570019-28051365-2567
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