Kerjaschki D, Miettinen A, Farquhar M G
J Exp Med. 1987 Jul 1;166(1):109-28. doi: 10.1084/jem.166.1.109.
The nephritogenic antigen of Heymann's nephritis (HN), gp330, was previously demonstrated (4-9) to be a resident glycoprotein of coated pits in the glomerular and proximal tubule epithelium of rats, and anti-gp330 IgG given intravenously was found to form IDs in glomeruli (passive HN). The purpose of this study was to investigate the detailed events that occur in the formation of IDs in passive HN. HN was induced by the injection of either 125I-labeled or unlabeled anti-gp330 IgG. At various times after injection (15 min to 8 d) the kidneys of some of the injected rats were fixed by perfusion, and the distribution of the rabbit IgG was determined by immunofluorescence and by immunoelectron microscopy. Glomeruli were isolated from the kidneys of injected rats and used for isolation of GBM fractions or for elution of the bound IgG. At 15 min to 1 h after injection, the rabbit IgG was localized by immunocytochemistry exclusively in coated pits along the podocyte plasmalemma facing the GBM. By 1-8 d, anti-gp330 IgG was detected in larger electron-dense IDs often located under the slit diaphragms. Serial sectioning revealed that each of the IDs maintained contact with a coated pit at some level. When GBMs isolated from rats given radiolabeled anti-gp330 IgG were examined by electron microscopy, the IDs were found to remain attached to the GBMs as early as 15 min after injection and coisolated with them at all time points. By double-immunolabeling of the isolated GBMs with two sizes of gold particles, both the antigen (gp330) and the anti-gp330 IgG could be demonstrated in IDs at all time points. When the amount of radiolabeled anti-gp330 bound to GBM fractions was compared with that of isolated glomeruli, it was found that 20% of the radiolabel remained bound to the purified GBMs at 15 min after injection, and 90% at 3 d. The bound IgG was released only by treatments that disrupt antibody-antigen complexes (high and low pH), but not by the other treatments we tried (detergent, high salt, heparinase, or collagenase digestion). When the IgG bound to glomeruli was eluted with acid citrate buffer 3 d after injection, it was found to specifically immunoprecipitate only gp330 from detergent-solubilized 125I-labeled kidney microvillar vesicles. By isoelectric focusing the eluate was found to be enriched in IgGs with acidic isoelectric points.(ABSTRACT TRUNCATED AT 400 WORDS)
海曼肾炎(HN)的致肾炎抗原gp330,先前已被证实(4 - 9)是大鼠肾小球和近端小管上皮细胞中被覆小窝的一种驻留糖蛋白,静脉注射抗gp330 IgG后发现其在肾小球中形成免疫沉积物(被动性HN)。本研究的目的是探究被动性HN中免疫沉积物形成过程中发生的详细事件。通过注射125I标记或未标记的抗gp330 IgG诱导HN。在注射后的不同时间点(15分钟至8天),对部分注射大鼠的肾脏进行灌注固定,通过免疫荧光和免疫电子显微镜确定兔IgG的分布。从注射大鼠的肾脏中分离出肾小球,用于分离肾小球基底膜(GBM)组分或洗脱结合的IgG。注射后15分钟至1小时,通过免疫细胞化学检测发现兔IgG仅定位在足细胞面向GBM的质膜上的被覆小窝中。到1 - 8天时,在通常位于裂孔隔膜下方的较大电子致密免疫沉积物中检测到抗gp330 IgG。连续切片显示,每个免疫沉积物在某种程度上都与一个被覆小窝保持接触。当对注射放射性标记抗gp330 IgG的大鼠分离得到的GBM进行电子显微镜检查时,发现免疫沉积物在注射后15分钟就已附着在GBM上,并在所有时间点都与GBM共同分离。通过用两种大小的金颗粒对分离的GBM进行双重免疫标记,在所有时间点的免疫沉积物中都能同时显示抗原(gp330)和抗gp330 IgG。当将与GBM组分结合的放射性标记抗gp330的量与分离的肾小球的量进行比较时,发现注射后15分钟时,20%的放射性标记仍与纯化的GBM结合,3天时为90%。结合的IgG仅通过破坏抗体 - 抗原复合物的处理(高pH和低pH)才能释放,而我们尝试的其他处理(去污剂、高盐、肝素酶或胶原酶消化)均不能使其释放。注射3天后用酸性柠檬酸盐缓冲液洗脱与肾小球结合的IgG时,发现其仅能从去污剂溶解的125I标记的肾微绒毛小泡中特异性免疫沉淀gp330。通过等电聚焦发现洗脱液中富含酸性等电点的IgG。(摘要截短于400字)