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类风湿关节炎中的 B 细胞:致病机制与治疗前景。

B Cells in Rheumatoid Arthritis:Pathogenic Mechanisms and Treatment Prospects.

机构信息

School of Basic Medical Sciences, Shanxi Medical University, Taiyuan, China.

Department of Rheumatology, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital, Third Hospital of Shanxi Medical University, Taiyuan, China.

出版信息

Front Immunol. 2021 Sep 28;12:750753. doi: 10.3389/fimmu.2021.750753. eCollection 2021.

Abstract

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 CD4T 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.

摘要

类风湿关节炎(RA)是一种常见的、慢性的、全身性自身免疫性疾病,其临床特征为关节滑膜组织增生、血管翳形成和软骨破坏。RA 的全球发病率约为 1%,且多见于女性。RA 的基本特征是机体免疫系统紊乱,其中 RA 患者体内的自身反应性 CD4T 细胞、致病性 B 细胞、M1 巨噬细胞、炎性细胞因子、趋化因子和自身抗体异常增加。B 细胞耗竭疗法已充分证明 B 细胞在 RA 发病机制中的重要作用,以 B 细胞作为靶点治疗 RA 也越来越受到关注。虽然接受 B 细胞耗竭疗法的 RA 患者的炎症指标有显著改善,但感染和癌症的风险也增加了,这表明我们需要耗竭致病性 B 细胞而不是所有 B 细胞。然而,目前我们无法区分 RA 患者中的致病性 B 细胞和保护性 B 细胞。本综述探讨了 B 细胞在 RA 发生、发展和治疗中的作用的新观点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5a9a/8505880/7e5876a9de89/fimmu-12-750753-g001.jpg

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