IgA肾病肠道黏膜免疫致病机制的再认识:肠源性IgA^(+)浆细胞

Recognition of intestinal mucosal immunopathogenesis of IgA nephropathy: gut-derived IgA+ plasma cells

肠源性IgA^(+)浆细胞是肠道黏膜免疫发挥免疫效应的关键。肠源性IgA^(+)浆细胞的产生受肠道菌群和饮食调控,不仅在肠道黏膜局部发挥免疫作用,还可迁徙至肠道外的组织或器官,通过依赖产生IgA抗体或分泌细胞因子等非抗体产生效应来调节免疫和炎症反应,在多种疾病中发挥免疫调节的保护或者致病效应。肠道黏膜免疫失衡在IgA肾病中的致病效应逐渐被关注。IgA肾病高血清IgA小鼠肠道固有层IgA^(+)浆细胞的增多与循环中异常糖基化IgA1增多有关。IgA肾病患者循环中的长寿命浆细胞数量增加,并抑制白细胞介素-6发挥致病作用。但肠源性IgA^(+)浆细胞是否迁移至肾脏局部促进疾病进展尚不清楚。现就肠源性IgA^(+)浆细胞在IgA肾病肠道黏膜免疫致病效应及机制的相关研究进展进行综述。

Gut-derived IgA+plasma cells are the key to intestinal mucosal immunity.The intestinal flora and diet regulate the production of gut-derived IgA+plasma cells,which not only play an immune role in the intestinal mucosa,but also migrate to tissues or organs outside the intestine to regulate immune and inflammatory reactions by relying on the production of IgA antibodies or the secretion of cytokines and other non-antibody effects,and act as a protective or pathogenic factor in various diseases.The pathogenic effect of intestinal mucosal immune imbalance in IgA nephropathy(IgAN)has been a concern.IgA+plasma cells increase in intestinal lamina propria of high serum IgA mice with the increase of abnormally glycosylated IgA1.The long-lived plasma cells increase,and interleukin-6 is inhibited in IgAN patients.However,it remains unclear whether gut-derived IgA+plasma cells migrate to kidneys to promote disease progression.This article reviews the relevant research progress on the immunopathologic effects and mechanisms of gut-derived IgA+plasma cells in the intestinal mucosa of IgAN.