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分子机制将干燥综合征的炎症与自身免疫联系起来:新靶点的鉴定。

Molecular Mechanisms Linking Inflammation to Autoimmunity in Sjögren's Syndrome: Identification of New Targets.

机构信息

Department of Translational Biomedicine and Neuroscience (DiBraiN), Section of Human Anatomy and Histology, University of Bari "Aldo Moro", Piazza Giulio Cesare 1, I-70124 Bari, Italy.

出版信息

Int J Mol Sci. 2022 Oct 30;23(21):13229. doi: 10.3390/ijms232113229.

DOI:10.3390/ijms232113229
PMID:36362017
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9658723/
Abstract

Sjögren's syndrome (SS) is a systemic autoimmune rheumatic disorder characterized by the lymphocytic infiltration of exocrine glands and the production of autoantibodies to self-antigens. The involvement of the exocrine glands drives the pathognomonic manifestations of dry eyes (keratoconjunctivitis sicca) and dry mouth (xerostomia) that define sicca syndrome. To date, the molecular mechanisms mediating pathological salivary gland dysfunction in SS remain to be elucidated, despite extensive studies investigating the underlying cause of this disease, hampering the development of novel therapeutic strategies. Many researchers have identified a multifactorial pathogenesis of SS, including environmental, genetic, neuroendocrine, and immune factors. In this review, we explore the latest developments in understanding the molecular mechanisms involved in the pathogenesis of SS, which have attracted increasing interest in recent years.

摘要

干燥综合征(SS)是一种系统性自身免疫性风湿病,其特征是外分泌腺的淋巴细胞浸润和自身抗原的自身抗体产生。外分泌腺的受累导致了干燥性角结膜炎(干眼症)和口干(口干燥症)的特征性表现,定义了干燥综合征。尽管广泛研究了这种疾病的根本原因,但到目前为止,介导 SS 病理性唾液腺功能障碍的分子机制仍有待阐明,这阻碍了新型治疗策略的发展。许多研究人员已经确定了 SS 的多因素发病机制,包括环境、遗传、神经内分泌和免疫因素。在这篇综述中,我们探讨了近年来理解 SS 发病机制中涉及的分子机制的最新进展,这些进展引起了越来越多的兴趣。

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