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原发性干燥综合征的发病机制超出 B 淋巴细胞。

Pathogenesis of primary Sjögren's syndrome beyond B lymphocytes.

机构信息

Division of Rheumatology, Department of Precision Medicine, University of Campania Luigi Vanvitelli, Naples, Italy.

Department of Pathology and Shenzhen Institute of Research and Innovation, The University of Hong Kong, China.

出版信息

Clin Exp Rheumatol. 2020 Jul-Aug;38 Suppl 126(4):315-323. Epub 2020 Oct 23.

Abstract

Primary Sjögren's syndrome (pSS) is a chronic autoimmune disorder affecting exocrine glands of the body, prevalently lacrimal and salivary glands. The pSS pathogenesis has been thought to be B-cell-centric and several clinical trials have been carried out in order to clarify the therapeutic role of B-cell depletion in patients with pSS. Unfortunately, however, B-cell depletion with rituximab has failed in demonstrating any significant results in pSS patients. Besides the contribution of B cells in the pathogenesis of pSS, effector Tfh, Th17 and Th22 cells, follicular dendritic cells (DCs), innate cells (ICs) and several cytokines, chemokines and miRNA have been proved to participate to the development of this systemic disease. Understanding these molecular processes may help guide research into resistant diseases and highly targeted therapeutic strategies. This review aims to discuss important pathogenetic mechanisms involved in the initiation and perpetuation of pSS behind the established role of B cells.

摘要

原发性干燥综合征(pSS)是一种慢性自身免疫性疾病,影响身体的外分泌腺,主要是泪腺和唾液腺。pSS 的发病机制被认为是以 B 细胞为中心的,已经进行了几项临床试验,以阐明 B 细胞耗竭在 pSS 患者中的治疗作用。然而,遗憾的是,用利妥昔单抗进行 B 细胞耗竭未能在 pSS 患者中显示出任何显著效果。除了 B 细胞在 pSS 发病机制中的作用外,效应性滤泡辅助性 T 细胞(Tfh)、Th17 和 Th22 细胞、滤泡树突状细胞(DC)、固有细胞(IC)和几种细胞因子、趋化因子和 miRNA 已被证明参与了这种全身性疾病的发展。了解这些分子过程可能有助于指导对耐药疾病和高度靶向治疗策略的研究。本文综述旨在讨论在已确立的 B 细胞作用之外,pSS 发病和持续的重要发病机制。

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