Sato T, Kawachi H, Morioka T, Takashima N, Saeki T, Oite T, Sato N L, Takeuchi M, Shimizu F
Department of Immunology, Niigata University School of Medicine, Japan.
Clin Exp Immunol. 1993 Jan;91(1):131-4. doi: 10.1111/j.1365-2249.1993.tb03367.x.
By immunization with rabbit immunoglobulins and the injection of a subnephritogenic dose of rabbit nephrotoxic serum (NTS), accelerated-type nephrotoxic serum nephritis (NTN) was induced in heterozygous (rnu/+) rats but not in athymic nude (rnu/rnu) rats. By transferring rat antibody against rabbit immunoglobulins, marked proteinuria was induced also in nude rats (202.0 +/- 98.4 mg/day on day 3) as in rnu/+ rats (122.6 +/- 35.3 mg/day on day 3). No marked differences in histological findings could be found between both groups. The most marked increase in the number of intraglomerular infiltrating cells was observed in heterozygous rats indicating that the presence of thymus-derived cells leads to the accumulation of more cells in glomeruli. We conclude that humoral immunity alone is enough to accelerate the pathogenic mechanism which induces glomerular injury with heavy proteinuria in this model.
通过用兔免疫球蛋白进行免疫并注射亚肾炎剂量的兔肾毒性血清(NTS),在杂合子(rnu/+)大鼠中诱导出加速型肾毒性血清肾炎(NTN),但在无胸腺裸鼠(rnu/rnu)中未诱导出。通过转移抗兔免疫球蛋白的大鼠抗体,无胸腺裸鼠(第3天为202.0±98.4毫克/天)也像杂合子大鼠(第3天为122.6±35.3毫克/天)一样诱导出明显的蛋白尿。两组之间在组织学结果上未发现明显差异。在杂合子大鼠中观察到肾小球内浸润细胞数量增加最为明显,这表明胸腺来源细胞的存在导致更多细胞在肾小球中积聚。我们得出结论,在该模型中,仅体液免疫就足以加速导致严重蛋白尿性肾小球损伤的致病机制。