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Nephrotoxic serum nephritis in nude rats: the roles of host immune reactions in the accelerated type.

机译:裸鼠肾毒性血清肾炎:宿主免疫反应在加速型中的作用。

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摘要

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.
机译:通过用兔免疫球蛋白免疫并注射亚肾炎剂量的兔肾毒性血清(NTS),在杂合性(rnu / +)大鼠中诱导了加速型肾毒性血清肾炎(NTN),而在无胸腺裸鼠(rnu / rnu)中则未诱导。通过转移针对兔免疫球蛋白的大鼠抗体,裸鼠(第3天为202.0 +/- 98.4 mg /天)也与rnu / +大鼠(第3天为122.6 +/- 35.3 mg /天)一样诱导明显的蛋白尿。两组之间在组织学结果上均无明显差异。在杂合大鼠中观察到肾小球内浸润细胞数量的最明显增加,表明胸腺来源的细胞的存在导致更多的细胞在肾小球中积累。我们得出的结论是,在此模型中,仅凭体液免疫就足以加速引起肾小球重蛋白尿损伤的致病机制。

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