Abstract
Regulatory T cells (Tregs) represent a distinct subpopulation of CD4+ T lymphocytes that promote immune tolerance and maintain immune system homeostasis. The dysfunction of Tregs is tightly associated with rheumatoid arthritis (RA). Although the complex pathogenic processes of RA remain unclear, studies on Tregs in RA have achieved substantial progress not only in fundamental research but also in clinical application. This review discusses the current knowledge of the characterizations, functions, and molecular mechanisms of Tregs in the pathogenesis of RA, and potential therapies for these disorders are also involved.
Highlights
Rheumatoid arthritis (RA) is a chronic and inflammatory autoimmune disease characterized by persistent synovitis, systemic inflammation, and symmetrical joint involvement
RA has been mainly treated with disease-modifying antirheumatic drugs (DMARDs), such as methotrexate and leflunomide, supplemented with nonsteroidal anti-inflammatory drugs (NSAIDs) and/or glucocorticoids to alleviate the condition, but it cannot be completely cured
As ligands for G protein–coupled receptors (GPCRs), short-chain fatty acids (SCFAs) induce the differentiation of Tregs and Tr1 cells by increasing the expression of forkhead box P3 (Foxp3) and upregulating the secretion of IL-10 and transforming growth factor (TGF)-β via GPCR41, GPCR43, and GPCR109 (Smith et al, 2013; Singh et al, 2014)
Summary
Rheumatoid arthritis (RA) is a chronic and inflammatory autoimmune disease characterized by persistent synovitis, systemic inflammation, and symmetrical joint involvement. After regulatory T cells (Tregs) were identified as a specific subpopulation with suppressive capacity maintaining immune homeostasis, numerous studies have related Treg disorders to RA. AhR regulates Treg differentiation and function in a ligand-specific fashion (Gandhi et al, 2010) through different mechanisms, such as direct functional enhancements, induction of epigenetic modifications of Foxp3, and modulation of dendritic cells (DCs) (Quintana, 2013).
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