摘要
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。
bjectiveForfurtherstudyofpathogenicmechanismofHeymannnephritis(HN)andsearchingforefectivetreatment.MethodsActiveHeymannnephritiswasinducedbyimmunizingLewisratwithacrudemembraneex-tract(FXIA)preparedfromrenalcorticaltubules.UrineproteinexcretionwasmonitoredtodeterminetheonsetofnephritisandthenthelymphcelsofnephritisratswerefusedwithamouseSP2/0myelomacelline.Supernatantsfromhybridomacultureswerescreenedforproductionofanti-gp330antibodybyenzyme-linkedimmunoassay(ELISA).Onerat/mousehybridomaC3-6whichwaspositivebyELISAwassubcloned.ResultsGradient5%～12%slabsodiumdodeccylsulphatepalyacrylamindegelsandwestern-blotshowedthatMcAbC3-6recognizedanapparentmassof330000peptidefromsolublizedFXIA.TheimmunedepositswerelocatedbetweenthepodocytecelsandGBMbydirectimmunoperoxidaseimmunoelectronmicroscopy.ConclusionMcAbC3-6isamonoclonalautoantibodyagainstgp330thatrecognizesthepathogenicepitopeongp330molecule.
出处
《中华肾脏病杂志》
CAS
CSCD
北大核心
1996年第6期343-346,共4页
Chinese Journal of Nephrology
基金
国家青年自然科学基金
