Naish P F, Thomson N M, Simpson I J, Peters D K
Clin Exp Immunol. 1975 Oct;22(1):102-11.
The role of polymorphonuclear leucocytes (PMN) in the autologous phase of nephrotoxic nephritis (NTN) in the rabbit has been investigated. Depletion of circulating PMN by nitrogen mustard protected renal function and immunofluorescent examination showed reduction in glomerular fibrin deposition. Depletion of circulating PMN using a highly specific goat anti-PMN serum (APS) provided similar protection of renal function, highly significant reduction in proteinuria and histological and immunofluorescent examination showed reduced glomerular PMN infiltration, extracapillary cell proliferation and virtual absence of fibrin deposition. Although protection by nitrogen mustard may have been partly due to immunosuppression, no reduction in antibody response was detected in the APS-treated rabbits. The results implicate the polymorph as the principal injurious agent in this model of NTN, responsible directly or indirectly for both proteinuria and glomerular fibrin deposition.
已对多形核白细胞(PMN)在兔肾毒性肾炎(NTN)自体阶段中的作用进行了研究。用氮芥消耗循环中的PMN可保护肾功能,免疫荧光检查显示肾小球纤维蛋白沉积减少。使用高度特异性的山羊抗PMN血清(APS)消耗循环中的PMN可提供类似的肾功能保护,蛋白尿显著减少,组织学和免疫荧光检查显示肾小球PMN浸润、毛细血管外细胞增殖减少且几乎没有纤维蛋白沉积。虽然氮芥的保护作用可能部分归因于免疫抑制,但在经APS处理的兔子中未检测到抗体反应降低。结果表明多形核白细胞是该NTN模型中的主要损伤因子,直接或间接导致蛋白尿和肾小球纤维蛋白沉积。