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为了进一步研究Ｈｅｙｍａｎｎ肾炎（ＨＮ）的病理损伤机制，发展有效的治疗手段。方法应用大鼠肾小管刷状缘抗原ＦＸＩＡ免疫近交系Ｌｅｗｉｓ大鼠，诱导了主动型ＨＮ模型。并用该ＨＮ大鼠的淋巴细胞与小鼠ＳＰ２／０骨髓瘤细胞融合，建立异种大鼠／小鼠之间的杂交瘤细胞株，产生了大鼠抗致病原Ｃ３－６自身单克隆抗体（ＭｃＡｂ）。结果ＳＤＳ－ＰＡＧＥ和Ｗｅｓｔｅｒｎ－Ｂｌｏｔ显示，ＭｃＡｂＣ３－６识别分子量为３３００００的刷状缘抗原。ＭｃＡｂＣ３－６诱导的被动型ＨＮ大鼠免疫组化和免疫电镜表明该ＭｃＡｂＣ３－６在体内识别肾小球基底膜上皮足突表面抗原，并与之结合形成免疫沉积，其识别的抗原分布与文献报导ｇｐ３３０抗原分布相似。结论证明ＭｃＡｂＣ３－６是针对致病原ｇｐ３３０的自身ＭｃＡｂ。
In order to further study the pathological injury mechanism of Heymann nephritis (HN), develop effective treatment. Methods The inbred Lewis rats were immunized with FGFR-1, and the active HN model was induced. The hybridoma cell lines between xenogeneic rat / mouse were established by fusing lymphocytes of the HN rat with mouse SP2 / 0 myeloma cells to produce rat anti-pathogenic C3-6 autoantibodies McAb). Results SDS-PAGE and Western-Blot showed that McAbC3-6 recognized the brush border antigen with a molecular weight of 330,000. McAbC3-6 induced passive HN rat immunohistochemistry and immunoelectron microscopy showed that the McAbC3-6 in vivo identification of glomerular basement membrane epithelial process surface antigen, and combined with the formation of immune deposition, the identification of the antigen distribution and the literature The distribution of gp330 antigens is reported to be similar. The conclusion proves that McAbC3-6 is a self-McAb against pathogenic gp330.