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免疫致病机制在小鼠自发性肾小球病中的作用。

Involvement of immunopathogenic mechanisms in a spontaneously occurring glomerulopathy in mice.

作者信息

Chen A, Sheu L F, Chou W Y, Ho Y S, Lin Y F, Lin F G, Lee W H

机构信息

Department of Pathology, Tri-Service General Hospital, Taipei, Taiwan, ROC.

出版信息

Nephron. 1998;78(1):63-72. doi: 10.1159/000044884.

DOI:10.1159/000044884
PMID:9453406
Abstract

Mice have been found to be susceptible to spontaneous renal localization of immune deposits. However, the significance of these immune deposits is still debated. We investigated the immunopathogenesis of a naturally occurring glomerulopathy associated with progressive proteinuria and glomerulosclerosis in 75 BALB/c mice. The mice were divided into five groups of 15 and killed at the age of 1, 3, 6, 12, or 18 months for laboratory and renal pathologic studies. These mice showed persistently increasing serum levels of immune complexes, a marked increase of glomerular immune deposits which were capable of fixing C3, and interstitial infiltration of lymphocytes and plasma cells, followed by the occurrence of proteinuria, mesangiopathy, and glomerulosclerosis. Our findings suggest that an immune system mediated process occurred in the kidneys of the mice tested.

摘要

已发现小鼠易发生免疫复合物的自发性肾脏定位。然而,这些免疫复合物的意义仍存在争议。我们研究了75只BALB/c小鼠中一种与进行性蛋白尿和肾小球硬化相关的自然发生的肾小球病的免疫发病机制。将小鼠分为五组,每组15只,在1、3、6、12或18月龄时处死,进行实验室和肾脏病理研究。这些小鼠的免疫复合物血清水平持续升高,能够固定C3的肾小球免疫沉积物显著增加,淋巴细胞和浆细胞间质浸润,随后出现蛋白尿、系膜病变和肾小球硬化。我们的研究结果表明,在受试小鼠的肾脏中发生了免疫系统介导的过程。

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