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[免疫球蛋白A血管炎的病因及发病机制研究进展]

[Research advances in the etiology and pathogenesis of immunoglobulin A vasculitis].

作者信息

Jianati Reaila, Liu Xi-Xi, Zhu Xue-Jun

机构信息

Department of Hematology, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing 210029, China (Zhu X-J, Email:

出版信息

Zhongguo Dang Dai Er Ke Za Zhi. 2023 Dec 15;25(12):1287-1292. doi: 10.7499/j.issn.1008-8830.2307065.

Abstract

Immunoglobulin A vasculitis (IgAV), also known as Henoch-Schönlein purpura, has complex etiology and pathogenesis which have not been fully clarified. The latest research shows that SARS-CoV-2 and related vaccines, human papilloma vaccine, and certain biological agents can also induce IgAV. Most studies believe that the formation of galactose-deficient IgA1 (Gd-IgA1) and Gd-IgA1-containing immune complex plays a crucial role in the pathogenesis of IgAV. It is hypothesized that the pathogenesis of IgAV is associated with the binding of IgA1 to anti-endothelial cell antibodies. In addition, genetics also constitutes a major focus of IgAV research. This article reviews the new advances in the etiology of IgAV and summarizes the role of Gd-IgA1, Gd-IgA1-containing immune complex, anti-endothelial antibody, IgA1 conjugates, T lymphocyte immunity, and genetic factors in the pathogenesis of IgAV.

摘要

免疫球蛋白A血管炎(IgAV),也称为过敏性紫癜,其病因和发病机制复杂,尚未完全阐明。最新研究表明,严重急性呼吸综合征冠状病毒2(SARS-CoV-2)及相关疫苗、人乳头瘤病毒疫苗和某些生物制剂也可诱发IgAV。大多数研究认为,缺乏半乳糖的IgA1(Gd-IgA1)和含Gd-IgA1的免疫复合物的形成在IgAV发病机制中起关键作用。据推测,IgAV的发病机制与IgA1与抗内皮细胞抗体的结合有关。此外,遗传学也是IgAV研究的一个主要重点。本文综述了IgAV病因学的新进展,并总结了Gd-IgA1、含Gd-IgA1的免疫复合物、抗内皮抗体、IgA1缀合物、T淋巴细胞免疫和遗传因素在IgAV发病机制中的作用。

相似文献

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[Research advances in the etiology and pathogenesis of immunoglobulin A vasculitis].[免疫球蛋白A血管炎的病因及发病机制研究进展]
Zhongguo Dang Dai Er Ke Za Zhi. 2023 Dec 15;25(12):1287-1292. doi: 10.7499/j.issn.1008-8830.2307065.
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Pathogenesis of IgA Vasculitis: An Up-To-Date Review.IgA 血管炎的发病机制:最新综述。
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Henoch-Schonlein Purpura in a Newly Diagnosed HIV Patient.一名新诊断出的艾滋病患者患过敏性紫癜。
Eur J Case Rep Intern Med. 2022 May 4;9(5):003363. doi: 10.12890/2022_003363. eCollection 2022.

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