Oite T, Batsford S R, Mihatsch M J, Takamiya H, Vogt A
J Exp Med. 1982 Feb 1;155(2):460-74. doi: 10.1084/jem.155.2.460.
Cationized human IgG can bind to the rat glomerular basement membrane (GBM), act as planted antigen, and induce in situ immune complex formation accompanied by severe glomerulonephritis. Perfusion of highly cationized human IgG (isoelectric point {more than} 9.5) via the left renal artery resulted in preferential localization within the perfused kidney (up to 56 percent of dose injected); after intravenous administration, only 4 percent was bound to the kidneys. The planted antigen was localized along the glomerular capillary walls and was accessible for antibody administered intravenously 1 h after perfusion, when virtually no antigen remained in the circulation. Persistence of cationized human IgG in the perfused kidney was markedly prolonged when complexed with antibody; one-half the cationized human IgG was still present after 12 d. There was a difference in the disappearance rates of antigen and antibody, as cationized human IgG was removed faster from the kidney than the antibody, the binding of which remained almost unchanged during the first week. Renal perfusion of a minimum of 20 mug of cationized human IgG, followed by intravenous injection of antibody, regularly induced severe glomerulonephritis with a proteinuria of at least 100 mg/24 h. The degree and the persistence of proteinuria induced depended on the dose of cationized human IgG perfused. Experiments using radiolabeled antigen and antibody showed that after renal perfusion of 20 mug cationized human IgG, 11.1 mug was kidney bound at the time of antibody injection. At the onset of proteinuria, 4.0 mug of antigen and 31.9 mug of anti-human IgG antibody were present in the perfused kidney. Immunofluorescence revealed immune deposits consisting of cationized human IgG and rabbit IgG (anti-human IgG) along the GBM. The staining pattern was linear (confluent) during the first 2 d and became granular during the course of the disease. Electronmicroscopically, a prominent finding was the accumulation of dense deposits, mainly in the subepithelial space and beneath the slit pores.
阳离子化人IgG可与大鼠肾小球基底膜(GBM)结合,作为植入抗原,并诱导原位免疫复合物形成,伴有严重的肾小球肾炎。通过左肾动脉灌注高度阳离子化的人IgG(等电点大于9.5)导致其优先定位在灌注的肾脏内(高达注射剂量的56%);静脉注射后,只有4%与肾脏结合。植入的抗原定位在肾小球毛细血管壁上,灌注后1小时静脉注射抗体时可与之结合,此时循环中几乎没有抗原残留。当与抗体复合时,阳离子化人IgG在灌注肾脏中的持续时间明显延长;12天后仍有一半的阳离子化人IgG存在。抗原和抗体的消失速率存在差异,因为阳离子化人IgG从肾脏中清除的速度比抗体快,抗体的结合在第一周几乎保持不变。至少灌注20μg阳离子化人IgG,随后静脉注射抗体,通常会诱导严重的肾小球肾炎,蛋白尿至少为100mg/24h。诱导的蛋白尿程度和持续时间取决于灌注的阳离子化人IgG剂量。使用放射性标记抗原和抗体的实验表明,在灌注20μg阳离子化人IgG后,抗体注射时肾脏结合了11.1μg。在蛋白尿开始时,灌注的肾脏中存在4.0μg抗原和31.9μg抗人IgG抗体。免疫荧光显示沿GBM有由阳离子化人IgG和兔IgG(抗人IgG)组成的免疫沉积物。在疾病的最初2天,染色模式为线性(融合),在病程中变为颗粒状。电子显微镜下,一个突出的发现是致密沉积物的积累,主要位于上皮下间隙和裂孔下方。