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      The Role of Different Subsets of Regulatory T Cells in Immunopathogenesis of Rheumatoid Arthritis

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          Abstract

          Rheumatoid arthritis (RA) is a common autoimmune disease and a systemic inflammatory disease which is characterized by chronic joint inflammation and variable degrees of bone and cartilage erosion and hyperplasia of synovial tissues. Considering the role of autoreactive T cells (particularly Th1 and Th17 cells) in pathophysiology of RA, it might be assumed that the regulatory T cells (Tregs) will be able to control the initiation and progression of disease. The frequency, function, and properties of various subsets of Tregs including natural Tregs (nTregs), IL-10-producing type 1 Tregs (Tr1 cells), TGF- β -producing Th3 cells, CD8 + Tregs, and NKT regulatory cells have been investigated in various studies associated with RA and collagen-induced arthritis (CIA) as experimental model of this disease. In this paper, we intend to submit the comprehensive information about the immunobiology of various subsets of Tregs and their roles and function in immunopathophysiology of RA and its animal model, CIA.

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          Naturally arising Foxp3-expressing CD25+CD4+ regulatory T cells in immunological tolerance to self and non-self.

          Shimon Sakaguchi (2005)
          Naturally arising CD25(+)CD4(+) regulatory T cells actively maintain immunological self-tolerance. Deficiency in or dysfunction of these cells can be a cause of autoimmune disease. A reduction in their number or function can also elicit tumor immunity, whereas their antigen-specific population expansion can establish transplantation tolerance. They are therefore a good target for designing ways to induce or abrogate immunological tolerance to self and non-self antigens.
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            A function for interleukin 2 in Foxp3-expressing regulatory T cells.

            Jason D. Fontenot, Jeffrey P. Rasmussen, Marc A Gavin … (2005)
            Regulatory T cells (T(reg) cells) expressing the forkhead family transcription factor Foxp3 are critical mediators of dominant immune tolerance to self. Most T(reg) cells constitutively express the high-affinity interleukin 2 (IL-2) receptor alpha-chain (CD25); however, the precise function of IL-2 in T(reg) cell biology has remained controversial. To directly assess the effect of IL-2 signaling on T(reg) cell development and function, we analyzed mice containing the Foxp3(gfp) knock-in allele that were genetically deficient in either IL-2 (Il2(-/-)) or CD25 (Il2ra(-/-)). We found that IL-2 signaling was dispensable for the induction of Foxp3 expression in thymocytes from these mice, which indicated that IL-2 signaling does not have a nonredundant function in the development of T(reg) cells. Unexpectedly, Il2(-/-) and Il2ra(-/-) T(reg) cells were fully able to suppress T cell proliferation in vitro. In contrast, Foxp3 was not expressed in thymocytes or peripheral T cells from Il2rg(-/-) mice. Gene expression analysis showed that IL-2 signaling was required for maintenance of the expression of genes involved in the regulation of cell growth and metabolism. Thus, IL-2 signaling seems to be critically required for maintaining the homeostasis and competitive fitness of T(reg) cells in vivo.
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              Thymic selection of CD4+CD25+ regulatory T cells induced by an agonist self-peptide.

              M. S. Jordan, A Boesteanu, A Reed … (2001)
              Despite accumulating evidence that regulatory T cells play a crucial role in preventing autoimmunity, the processes underlying their generation during immune repertoire formation are unknown. We show here that interactions with a single self-peptide can induce thymocytes that bear an autoreactive T cell receptor (TCR) to undergo selection to become CD4+CD25+ regulatory T cells. Selection of CD4+CD25+ thymocytes appears to require a TCR with high affinity for a self peptide because thymocytes that bear TCRs with low affinity do not undergo selection into this pathway. Our findings indicate that specificity for self-peptides directs the selection of CD4+CD25+ regulatory thymocytes by a process that is distinct from positive selection and deletion.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Arthritis
                Journal ID (iso-abbrev): Arthritis
                Journal ID (publisher-id): ARTH
                Title: Arthritis
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 2090-1984
                ISSN (Electronic): 2090-1992
                Publication date (Print): 2012
                Publication date (Electronic): 24 October 2012
                Volume: 2012
                Electronic Location Identifier: 805875
                Affiliations
                1Department of Immunology, School of Public Health, Tehran University of Medical Sciences, P.O. Box 6446, Tehran 14155, Iran
                2Imam Hassan Mojtaba Hospital, Alborz University of Medical Sciences, Karaj, Iran
                Author notes

                Academic Editor: Ruben Burgos-Vargas

                Article
                DOI: 10.1155/2012/805875
                PMC ID: 3486158
                PubMed ID: 23133752
                SO-VID: 33021e1d-71e7-4e02-b8eb-5b15ab796d20
                Copyright © Copyright © 2012 Maryam Gol-Ara et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 21 July 2012
                Date revision received : 11 September 2012
                Date accepted : 20 September 2012
                Categories
                Subject: Review Article

                ScienceOpen disciplines: Rheumatology
                Data availability:
                ScienceOpen disciplines: Rheumatology

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