Matsuda S, Czerkinsky C, Moldoveanu Z, Mestecky J
Department of Microbiology, University of Alabama at Birmingham.
Adv Exp Med Biol. 1987;216B:1577-81.
RBCs from one-third of IgA nephropathy patients examined had more IgA1 on their surface than cells from healthy volunteers. The amount of IgA1 on RBCs was estimated to be no more than 30 ng/4 x 10(8) RBCs. The level of IgG on the surface of RBCs from IgA nephropathy patients were the same as those from healthy volunteers. Free IgA1 myeloma protein binds poorly in vitro to RBCs from both an IgA deficient patient and healthy volunteers. Polyethylene glycol precipitate from the sera of IgA nephropathy patients bound to RBCs from an IgA deficient patient. Factor I did not release IgA1 bound to RBCs from IgA nephropathy patients. These results suggest that this binding is mediated through the interaction of IgA1 and RBCs, and that some alteration of the IgA1 molecule (complexes or aggregation) may account for this binding.
在接受检查的三分之一的IgA肾病患者中，其红细胞表面的IgA1比健康志愿者的细胞更多。红细胞上IgA1的量估计不超过30 ng/4×10⁸个红细胞。IgA肾病患者红细胞表面的IgG水平与健康志愿者的相同。游离的IgA1骨髓瘤蛋白在体外与IgA缺乏患者和健康志愿者的红细胞结合不佳。IgA肾病患者血清中的聚乙二醇沉淀物与IgA缺乏患者的红细胞结合。因子I不能从IgA肾病患者与红细胞结合的IgA1中释放出来。这些结果表明，这种结合是通过IgA1与红细胞的相互作用介导的，并且IgA1分子的某些改变（复合物或聚集）可能是这种结合的原因。
