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Indexed/Abstracted in: Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 1,236
Online ISSN 1827-1669
Wang D. 1, Li Y. 2, Liu Y. 2, Shi G. 2
1 Molecular Biology Research Center, Shandong Medical College, Linyi, Shandong, China;
2 Department of Rheumatology and Clinical Immunology, The First Affiliated Hospital of Xiamen University, Xiamen, Fujian, China
Rheumatoid arthritis (RA) is a systemic autoimmune disease characterised by chronic inflammation of joint synovial tissue and subsequent destruction of associated bone, cartilage and soft tissues. RA is commonly treated with non-steroidal anti-inflammatory drugs (NSAIDs), traditional disease-modifying antirheumatic drugs (DMARDs), glucocorticoids and biologic inhibitors of TNF, IL-1, IL-6, T cells and B cells. The use of these drugs especially biological agents has greatly improved the treatment of RA. Although the pathogenesis of RA remains unclear, T-cell mediated immune response is considered as a critical contributor in RA initiation and progression. It has been hypothesized that arthritogenic T cells (autoreactive T cells) escaping negative selection can recognize arthritogenic antigens and lead to autoimmunity and tissue destruction. Due to the important role of autoreactive T cells in the mechanisms of RA, they might be a novel therapeutic target. Many vaccines targeting autoreactive T cells which can establish immunological self tolerance have been developed. The efficacy of these vaccines has been justified in experimental models of RA and clinical trials. Inhibition of autoreactive T cell response by vaccination might provide a new treatment opinion in RA.