自身免疫性疾病中的 B 细胞消耗。

IF 20.3 1区 医学 Q1 RHEUMATOLOGY
Georg Schett, György Nagy, Gerhard Krönke, Dirk Mielenz
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引用次数: 0

摘要

B 细胞在类风湿性关节炎、多发性硬化症和系统性红斑狼疮等自身免疫性疾病的发病机制中起着关键作用。在自身免疫性疾病中,B 细胞协调抗原呈递、细胞因子的产生和自身抗体的产生,后者通过分化为分泌抗体的浆细胞和浆细胞来实现。本文探讨了目前消耗 B 细胞以改善甚至治愈自身免疫性疾病的治疗策略。文章探讨了用于治疗方法的 B 细胞系主要靶抗原。此外,它还总结了目前利用针对 B 细胞的单克隆抗体成功治疗自身免疫性疾病的证据,以及这些方法的局限性和挑战。最后,还讨论了嵌合抗原受体 T 细胞深度消耗 B 细胞和免疫重置的概念,以及从这种方法中吸取的经验教训,以便更好地理解 B 细胞在自身免疫性疾病中的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
B-cell depletion in autoimmune diseases.

B cells have a pivotal function in the pathogenesis of autoimmune diseases, such as rheumatoid arthritis, multiple sclerosis and systemic lupus erythematosus. In autoimmune disease, B cells orchestrate antigen presentation, cytokine production and autoantibody production, the latter via their differentiation into antibody-secreting plasmablasts and plasma cells. This article addresses the current therapeutic strategies to deplete B cells in order to ameliorate or potentially even cure autoimmune disease. It addresses the main target antigens in the B-cell lineage that are used for therapeutic approaches. Furthermore, it summarises the current evidence for successful treatment of autoimmune disease with monoclonal antibodies targeting B cells and the limitations and challenges of these approaches. Finally, the concept of deep B-cell depletion and immunological reset by chimeric antigen receptor T cells is discussed, as well as the lessons from this approach for better understanding the role of B cells in autoimmune disease.

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来源期刊
Annals of the Rheumatic Diseases
Annals of the Rheumatic Diseases 医学-风湿病学
CiteScore
35.00
自引率
9.90%
发文量
3728
审稿时长
1.4 months
期刊介绍: Annals of the Rheumatic Diseases (ARD) is an international peer-reviewed journal covering all aspects of rheumatology, which includes the full spectrum of musculoskeletal conditions, arthritic disease, and connective tissue disorders. ARD publishes basic, clinical, and translational scientific research, including the most important recommendations for the management of various conditions.
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