Nagy J, Scott H, Brandtzaeg P
Laboratory for Immunohistochemistry and Immunopathology, University of Oslo, Rikshospitalet, Norway.
Clin Nephrol. 1988 Jun;29(6):275-9.
It has been postulated that IgA NP is caused by mesangial deposition of IgA-containing immune complexes formed by IgA polymers (pIgA) which are overproduced in response to antigens presented at mucosal surfaces. The intestinal mucosa is one possible source of this pIgA. To test whether antibodies to dietary antigens might be involved in the pathogenesis of IgA NP, we measured IgG and IgA serum antibody activities to gluten, a gluten fraction called glyc-gli, alpha-lactalbumin, beta-lactoglobulin, casein and ovalbumin in 54 patients with IgA NP by an enzyme-linked immunosorbent assay (ELISA). The IgA activities to gluten antigens and alpha-lactalbumin were significantly increased in IgA NP compared with a group of 40 age-matched healthy controls. In a previous study we found that 4 out of 12 patients with IgA NP and gastrointestinal complaints had subtotal villous atrophy; this indicated that many patients with IgA NP have altered intestinal permeability which may lead to activation of their intestinal immune system. Taken together our results showed a relation between the intestinal humoral immune system and IgA NP and indicated that antibodies to dietary antigens in some patients may be directly involved in the pathogenesis of IgA NP.
据推测,IgA肾病是由含IgA的免疫复合物在系膜沉积所致,这些免疫复合物由IgA聚合物(pIgA)形成,pIgA是对黏膜表面呈现的抗原产生过度应答而产生的。肠黏膜是这种pIgA的一个可能来源。为了检测针对饮食抗原的抗体是否可能参与IgA肾病的发病机制,我们通过酶联免疫吸附测定(ELISA)检测了54例IgA肾病患者血清中针对麸质、一种名为糖基化麦醇溶蛋白的麸质组分、α-乳白蛋白、β-乳球蛋白、酪蛋白和卵清蛋白的IgG和IgA抗体活性。与40名年龄匹配的健康对照相比,IgA肾病患者针对麸质抗原和α-乳白蛋白的IgA活性显著升高。在先前的一项研究中,我们发现12例有胃肠道症状的IgA肾病患者中有4例存在绒毛萎缩;这表明许多IgA肾病患者存在肠道通透性改变,这可能导致其肠道免疫系统激活。综合我们的结果显示肠道体液免疫系统与IgA肾病之间存在关联,并表明部分患者针对饮食抗原的抗体可能直接参与IgA肾病的发病机制。