IgA肾病的遗传易感性和黏膜免疫应答异常

The recent research of pathogenesis of IgA nephropathy

众所周知,遗传风险因素和黏膜免疫异常在IgA肾病致病机制中起重要作用。近年来,系列研究已发现新的IgA肾病易感遗传位点,以及遗传风险因素和IgA肾病各方面,包括起病、临床表现、组织病理学、对治疗反应和预后之间的新关系。与此同时,肠道黏膜免疫异常在IgA肾病致病中的作用重新引起了人们的关注。肠道免疫耐受缺陷会削弱机体对微生物肠道屏障功能、增加食物抗原和细菌毒素的吸收、激活黏膜相关淋巴组织导致亚临床肠道炎症。遗传致病机制的进一步阐明和"肠道-肾关系"学说赋予IgA肾病新的治疗理念,如治疗亚临床肠道炎症或调控肠道微生物菌群,也利于进一步探索干预IgA的新靶目标和更加个体化的治疗。

It is known that genetic risk factors and mucosal immunity play vary important role in the pathogenesis of IgA nephropathy（ IgAN）. Recent years,new susceptibility loci of IgAN and relationships among genetic risk factors and each field of IgAN,which includes onset,clinical manifestation,histopathology,response to treatment and prognosis,have been found. Meanwhile,a resurgence of interest has addressed the role of intestinal immunity facing dietary components,like gluten or the complex intestinal flora,the microbiota. A defective immune tolerance might favor an abnormal response to microbiota with alterations of the intestinal barrier,including increased alimentary antigens and bacterial toxins absorption,triggering mucosal-associated lymphoid tissue（ MALT） activation and subclinical intestinal inflammation. The genetic pathogenesis and the new hypothesis for a strong intestine-kidney connection in IgAN are tempting,because they offer new treatment options,such as targeted to subclinical intestinal inflammation or microbiota modifications,and favor for further exploring new targets of IgAN intervention.