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免疫复合物与抗原诱导性关节炎兔胫骨软骨的有害相互作用。II:软骨细胞降解。

Deleterious interactions of immune complexes with tibial cartilage of antigen-induced arthritic rabbits. II: Chondrocyte degradation.

作者信息

Sumi M, Maeda M, Cooke T D

出版信息

Clin Orthop Relat Res. 1986 Nov(212):260-74.

PMID:2945686
Abstract

The observations of immune complex (IC) deposition in the surface of rheumatoid arthritis (RA) cartilage, in conjunction with degradative changes in superficial and midzone chondrocytes, raised the question of causal relationships. In antigen-induced arthritis in rabbits, cartilage degradation occurred in association with IC deposition and is accompanied by chondrocyte damage. Superficial and midzone chondrocytes in rabbit tibial cartilage of arthritic joints, induced by bovine serum albumin (BSA) or ferritin (Fn), were examined by electron microscopy during the evolution of the arthus response. The first cell changes were noted at six hours, by which time superficially formed IC had begun to extend into the matrix. Elongated cytoplasmic footlets, numerous lysosomes, and lipid droplets occurred initially. By 24 hours, concomitant with the deeper extension of surface IC, prominent changes in chondrocytes of both superficial, and midzones progressed to ultrastructural evidence of cell death. The pinocytosis of electron-dense amorphous materials, which included IC, preceded degradation. These data suggest that the observed cytopathology is a manifestation of locally deposited IC.

摘要

类风湿关节炎(RA)软骨表面免疫复合物(IC)沉积的观察结果,连同表层和中层软骨细胞的降解变化,引发了因果关系的问题。在兔抗原诱导性关节炎中,软骨降解与IC沉积相关,并伴有软骨细胞损伤。在阿瑟斯反应的演变过程中,通过电子显微镜检查了由牛血清白蛋白(BSA)或铁蛋白(Fn)诱导的关节炎关节兔胫骨软骨中的表层和中层软骨细胞。在6小时时首次注意到细胞变化,此时表层形成的IC已开始延伸到基质中。最初出现伸长的细胞质足突、大量溶酶体和脂滴。到24小时时,随着表面IC向更深层扩展,表层和中层软骨细胞的显著变化发展为细胞死亡的超微结构证据。电子致密无定形物质(包括IC)的胞饮作用先于降解。这些数据表明,观察到的细胞病理学是局部沉积IC的一种表现。

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