Iskandar S S, Jennette J C, Wilkman A S, Becker R L
Lab Invest. 1982 Mar;46(3):344-51.
Swiss albino, BALB/c, and eight substrains of C3H mice were given daily intraperitoneal injections of horse apoferritin (HAF) for up to 56 days. At varying intervals, renal tissue was examined by light, immunofluorescence, and electron microscopy. Swiss mice developed proliferative glomerulonephritis after 7 to 14 days of HAF, and 45 per cent progressed to severe crescentic glomerulonephritis after from 21 to 56 days of HAF. In Swiss mice, glomerular immune deposits evolved from predominantly IgM mesangial deposits at 7 days to mesangial IgG at 14 days to capillary wall IgG after 21 or more days of HAF injections. BALB/c mice given identical HAF doses never developed severe crescentic glomerulonephritis but rather an extensive global necrotizing glomerulonephritis most prevalent after from 9 to 18 days of HAF. The distinct evolution of glomerular immune deposits observed in Swiss mice was less clear-cut in BALB/c mice, with greater persistence of mesangial deposits and IgM over time. Only 11 per cent of C3H mice (confined to two substrains) developed glomerular lesions by light microscopy after 2 to 3 weeks of HAF administration. No C3H/HeN mice developed glomerulonephritis even after up to 47 days of HAF injection. From 7 days on, 45 per cent of HAF-injected C3H mice had low level IgM mesangial immune deposits but did not manifest the evolution from mesangial to capillary deposition observed in BALB/c and Swiss albino mice. F1 hybrid and congenic mice carrying BALB/c H-2 genetic information developed glomerular lesions similar to those produced in BALB/c mice. These data (1) indicate an interrelated morphologic and immunohistologic evolution of heterologous protein induced glomerular lesions in mice, (2) demonstrate morphologic and immunohistologic differences in glomerular lesions development between genetically disparate mouse strains given identical antigen exposures, and (3) support the genetic control of heterologous protein-induced glomerulonephritis and suggest a role for the major histocompatibility region in this genetic regulation.
将瑞士白化小鼠、BALB/c小鼠以及C3H小鼠的八个亚系每日腹腔注射马脱铁铁蛋白（HAF），持续56天。在不同时间间隔，通过光学显微镜、免疫荧光显微镜和电子显微镜检查肾脏组织。瑞士小鼠在注射HAF 7至14天后出现增殖性肾小球肾炎，45%在注射HAF 21至56天后进展为严重的新月体性肾小球肾炎。在瑞士小鼠中，肾小球免疫沉积物从注射HAF 7天时主要为IgM系膜沉积物，发展到14天时为系膜IgG，注射HAF 21天或更长时间后为毛细血管壁IgG。给予相同HAF剂量的BALB/c小鼠从未发展为严重的新月体性肾小球肾炎，而是出现广泛的全肾小球坏死性肾小球肾炎最常见于注射HAF 9至18天后。在瑞士小鼠中观察到的肾小球免疫沉积物的明显演变在BALB/c小鼠中不太明显，系膜沉积物和IgM随时间持续存在的情况更明显。在给予HAF 2至3周后，只有11%的C3H小鼠（局限于两个亚系）通过光学显微镜出现肾小球病变。即使注射HAF长达47天，也没有C3H/HeN小鼠发生肾小球肾炎。从7天起，45%注射HAF的C3H小鼠有低水平的IgM系膜免疫沉积物，但没有表现出在BALB/c和瑞士白化小鼠中观察到的从系膜沉积到毛细血管沉积的演变。携带BALB/c H-2遗传信息的F1杂种小鼠和同源近交系小鼠出现的肾小球病变与BALB/c小鼠产生的病变相似。这些数据（1）表明小鼠中异种蛋白诱导的肾小球病变在形态学和免疫组织学上存在相互关联的演变，（2）证明在相同抗原暴露下，遗传上不同的小鼠品系在肾小球病变发展方面存在形态学和免疫组织学差异，（3）支持异种蛋白诱导的肾小球肾炎受遗传控制，并表明主要组织相容性区域在这种遗传调控中起作用。
