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      Cells of the synovium in rheumatoid arthritis. T lymphocytes

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          Abstract

          Recent findings have substantiated the importance of T lymphocytes to the pathogenesis of rheumatoid arthritis (RA). Here, we review emerging data regarding genetic predisposition, spontaneous animal models of arthritis, and cell-cell interactions that implicate T cells as driving synovial inflammation and joint destruction. Information regarding the proinflammatory role of interleukin-17-producing T cells and the functional state of regulatory T cells both in animal models and in patients with RA is also discussed. In light of the overwhelming evidence that disrupted T-cell homeostasis greatly contributes to joint pathology in RA, the therapeutic potential of targeting activators of pro-inflammatory T cells or their products is compelling.

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          TGFbeta in the context of an inflammatory cytokine milieu supports de novo differentiation of IL-17-producing T cells.

          Marc Veldhoen, Richard J Hocking, Christopher Atkins … (2006)
          We describe de novo generation of IL-17-producing T cells from naive CD4 T cells, induced in cocultures of naive CD4 T cells and naturally occurring CD4+ CD25+ T cells (Treg) in the presence of TLR3, TLR4, or TLR9 stimuli. Treg can be substituted by TGFbeta1, which, together with the proinflammatory cytokine IL-6, supports the differentiation of IL-17-producing T cells, a process that is amplified by IL-1beta and TNFalpha. We could not detect a role for IL-23 in the differentiation of IL-17-producing T cells but confirmed its importance for their survival and expansion. Transcription factors GATA-3 and T-bet, as well as its target Hlx, are absent in IL-17-producing T cells, and they do not express the negative regulator for TGFbeta signaling, Smad7. Our data indicate that, in the presence of IL-6, TGFbeta1 subverts Th1 and Th2 differentiation for the generation of IL-17-producing T cells.
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            Transforming growth factor-beta regulation of immune responses.

            Ming Li, Yisong Y Wan, Shomyseh Sanjabi … (2006)
            Transforming growth factor-beta (TGF-beta) is a potent regulatory cytokine with diverse effects on hemopoietic cells. The pivotal function of TGF-beta in the immune system is to maintain tolerance via the regulation of lymphocyte proliferation, differentiation, and survival. In addition, TGF-beta controls the initiation and resolution of inflammatory responses through the regulation of chemotaxis, activation, and survival of lymphocytes, natural killer cells, dendritic cells, macrophages, mast cells, and granulocytes. The regulatory activity of TGF-beta is modulated by the cell differentiation state and by the presence of inflammatory cytokines and costimulatory molecules. Collectively, TGF-beta inhibits the development of immunopathology to self or nonharmful antigens without compromising immune responses to pathogens. This review highlights the findings that have advanced our understanding of TGF-beta in the immune system and in disease.
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              Suppression of immune induction of collagen-induced arthritis in IL-17-deficient mice.

              Susumu Nakae, Aya Nambu, Katsuko Sudo … (2003)
              Interleukin-17 is a T cell-derived proinflammatory cytokine. This cytokine is suspected to be involved in the development of rheumatoid arthritis (RA) because this cytokine expression is augmented in synovial tissues of RA patients. The pathogenic roles of IL-17 in the development of RA, however, still remain to be elucidated. In this study, effects of IL-17 deficiency on collagen-induced arthritis (CIA) model were examined using IL-17-deficient mice (IL-17(-/-) mice). We found that CIA was markedly suppressed in IL-17(-/-) mice. IL-17 was responsible for the priming of collagen-specific T cells and collagen-specific IgG2a production. Thus, these observations suggest that IL-17 plays a crucial role in the development of CIA by activating autoantigen-specific cellular and humoral immune responses.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Arthritis Res Ther
                Title: Arthritis Research & Therapy
                Publisher: BioMed Central (London )
                ISSN (Print): 1478-6354
                ISSN (Electronic): 1478-6362
                Publication date (Print): 2007
                Publication date (Electronic): 13 February 2007
                Volume: 9
                Issue: 1
                Page: 202
                Affiliations
                [1 ]Department of Internal Medicine, Division of Rheumatology and Rheumatic Diseases Core Center, University of Michigan Medical School, 4043 Biomedical Sciences Research Bldg., 109 Zina Pitcher Pl., Ann Arbor, MI 48109-2200, USA
                Article
                Publisher ID: ar2107
                DOI: 10.1186/ar2107
                PMC ID: 1860060
                PubMed ID: 17306038
                SO-VID: c2ff5d2f-3167-4ba4-9aac-0c1775b8a754
                Copyright © Copyright © 2007 BioMed Central Ltd
                History
                Categories
                Subject: Review

                ScienceOpen disciplines: Orthopedics
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                ScienceOpen disciplines: Orthopedics

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