免疫球蛋白A血管炎（immunoglobulin A vasculitis, IgAV），也称过敏性紫癜，病因及发病机制较为复杂，目前尚未完全阐明。最新研究表明，新型冠状病毒及相关疫苗、人乳头瘤疫苗及其他生物制剂等也可以诱发IgAV。大多研究认为，半乳糖缺陷型IgA1（galactose-deficient IgA1, Gd-IgA1）及含Gd-IgA1的免疫复合物形成在IgAV发病机制中起至关重要的作用。也有假设提出IgAV的发生与IgA1和抗内皮细胞抗体的结合有关。此外，遗传学也是IgAV研究的重点。该文综述IgAV病因的新进展，并总结Gd-IgA1、含Gd-IgA1的免疫复合物、抗内皮细胞抗体和IgA1的结合物、T细胞免疫及遗传因素在IgAV发病机制中的作用。

Immunoglobulin A vasculitis (IgAV), also known as Henoch-Sch?nlein 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.