B Cells in Rheumatoid Arthritis:Pathogenic Mechanisms and Treatment Prospects

Rheumatoid arthritis (RA) is a common, chronic, systemic autoimmune disease, and its clinical features are the proliferation of joint synovial tissue, the formation of pannus and the destruction of cartilage. The global incidence of RA is about 1%, and it is more common in women. The basic feature o...

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Published inFrontiers in immunology Vol. 12; p. 750753
Main Authors Wu, Fengping, Gao, Jinfang, Kang, Jie, Wang, Xuexue, Niu, Qing, Liu, Jiaxi, Zhang, Liyun
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Media S.A 28.09.2021
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Summary:Rheumatoid arthritis (RA) is a common, chronic, systemic autoimmune disease, and its clinical features are the proliferation of joint synovial tissue, the formation of pannus and the destruction of cartilage. The global incidence of RA is about 1%, and it is more common in women. The basic feature of RA is the body's immune system disorders, in which autoreactive CD4 T cells, pathogenic B cells, M1 macrophages, inflammatory cytokines, chemokines and autoantibodies abnormally increase in the body of RA patients B cell depletion therapy has well proved the important role of B cells in the pathogenesis of RA, and the treatment of RA with B cells as a target has also been paid more and more attention. Although the inflammatory indicators in RA patients receiving B-cell depletion therapy have been significantly improved, the risk of infection and cancer has also increased, which suggests that we need to deplete pathogenic B cells instead of all B cells. However, at present we cannot distinguish between pathogenic B cells and protective B cells in RA patients. In this review, we explore fresh perspectives upon the roles of B cells in the occurrence, development and treatment of RA.
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Edited by: Attila Mócsai, Semmelweis University, Hungary
Reviewed by: Changrong Ge, Karolinska Institutet (KI), Sweden; Nathalie Balandraud, Assistance publique des hôpitaux de Marseille AP-HM, France
These authors have contributed equally to this work and share first authorship
This article was submitted to Autoimmune and Autoinflammatory Disorders, a section of the journal Frontiers in Immunology
ISSN:1664-3224
1664-3224
DOI:10.3389/fimmu.2021.750753