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MRL/1小鼠类风湿关节炎样疾病的病因发病机制:II. 关节破坏的超微结构基础

Etiopathogenesis of rheumatoid arthritis-like disease in MRL/1 mice: II. Ultrastructural basis of joint destruction.

作者信息

Tanaka A, O'Sullivan F X, Koopman W J, Gay S

机构信息

Institute of Dental Research, University of Alabama, Birmingham.

出版信息

J Rheumatol. 1988 Jan;15(1):10-6.

PMID:3351831
Abstract

MRL/1 mice develop a spontaneous hindlimb arthropathy characterized by proliferation of synovial cells and by dissociation between early destruction of articular tissue and the presence of inflammatory cell infiltration. To characterize the ultrastructural details of the synovial cells of these mice, knee joints from MRL/1, MRL/n, and BALB/c mice were examined by light and electron microscopy. Since the proliferating synovial cells of MRL/1 mice resemble the previously described proliferative synovial cells seen in histopathologic specimens from early rheumatoid arthritis, further study of these cells may provide new insights into the pathogenesis of early joint tissue destruction in human rheumatic disease.

摘要

MRL/1小鼠会自发出现后肢关节病,其特征为滑膜细胞增殖,以及关节组织早期破坏与炎症细胞浸润的存在之间的分离。为了表征这些小鼠滑膜细胞的超微结构细节,通过光学显微镜和电子显微镜检查了来自MRL/1、MRL/n和BALB/c小鼠的膝关节。由于MRL/1小鼠增殖的滑膜细胞类似于先前在早期类风湿性关节炎组织病理学标本中所见的增殖性滑膜细胞,对这些细胞的进一步研究可能会为人类风湿性疾病早期关节组织破坏的发病机制提供新的见解。

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