摘要
IgA在过敏性紫癜（HSP）发病过程中起重要作用,目前研究显示HSP以IgA（主要是IgA1）在皮肤小血管壁和肾小球沉积为特征,而IgA1糖基化的水平降低.这种异常糖基化IgA1由于易于自身聚集,不易被肝细胞去唾液酸糖蛋白受体清除,削弱了补体清除免疫复合物的能力,以及暴露了新表位等原因,导致IgA1免疫复合物形成而沉积在皮肤血管壁及肾小球,主要经旁路途径激活补体,引起炎症损伤.此外,抗内皮细胞抗体、抗心磷脂抗体、抗中性粒细胞胞质抗体等各种IgA自身抗体也参与HSP的组织损伤过程.
IgA plays an important role in the course of Henoch-Schonlein purpura.The current study shows that the HSP is characterized by IgA principally IgA1） depositions in the wall of dermal vessel and the renal mesangium, and IgA1 is deficient in galactose. IgA1 with aberrant glycosylation has a tendency to be self-aggregated, not to be efficiently cleared by the hepatic asialoglycoprotein receptor. It also weakens the ability of complement to remove immune complexes, and causes the exposure of new epitope and so on. All these lead to the formation of IgA1 immune complexes and the deposition in the wall of dermal vessel and the renal mesangium. IgA1 immune complexes activate complement principally through the alternative pathway, which causes inflammatory injury. In addition, various IgA autoantibodies, such as anti-endothelial cell antibodies,anticardiolipin antibodies and anti-neutrophil cytoplasmic antibodies, are also involved in the process of tissue damage of Henoch-Schonlein purpura.
出处
《国际儿科学杂志》
2010年第5期478-480,共3页
International Journal of Pediatrics
