Synovial Tissue Inflammation Mediated by Autoimmune T Cells

Frontiers in Immunology

Yusuke Takeuchi¹  Keiji Hirota²  Shimon Sakaguchi³ 

[1] Department of Rheumatology and Clinical Immunology, Graduate School of Medicine, Kyoto University, Kyoto, Japan;Laboratory of Experimental Immunology, Immunology Frontier Research Center, Osaka University, Osaka, Japan;Laboratory of Experimental Immunology, Institute for Frontier Life and Medical Sciences, Kyoto University, Kyoto, Japan;Laboratory of Integrative Biological Science, Institute for Frontier Life and Medical Sciences, Kyoto University, Kyoto, Japan;

关键词: autoimmune arthritis;    Th17;    treg cells;    rheumatoid arthritis;    synovial inflammation;    proinflammatory cytokine;   

DOI  :  10.3389/fimmu.2019.01989

来源: DOAJ

【 摘 要 】

In rheumatoid arthritis (RA), various hematopoietic and non-hematopoietic cells present in the synovial tissue secrete numerous inflammatory mediators including pro-inflammatory cytokines critical for the induction of chronic joint inflammation and bone destruction. Fibroblast-like synoviocytes (FLSs) in the non-hematopoietic cell compartment are key inflammatory cells activated in inflamed joints and driving the disease; yet how synovial tissue inflammation is modulated by autoimmune T cells is not fully understood. In this review, mainly based on recent findings with a mouse model of spontaneous autoimmune arthritis, we discuss the mechanism of Th17-mediated synovial tissue inflammation; that is, what environmental stimuli and arthritogenic self-antigens trigger arthritis, how arthritogenic T cells initiate joint inflammation by stimulating FLSs, and how the cellular sources of GM-CSF from lymphoid and tissue stromal cells in the synovium contribute to the development of arthritis. We also highlight possible plasticity of Th17 cells toward pathogenic GM-CSF producers, and the functional instability of regulatory T cells under inflammatory conditions in RA joints.

【 授权许可】

Unknown