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米色(切迪阿克-希加什)小鼠的抗原诱导性关节炎。

Antigen induced arthritis in beige (Chediak-Higashi) mice.

作者信息

Schalkwijk J, Joosten L A, van den Berg W B, van de Putte L B

机构信息

Department of Rheumatology, University Hospital St Radboud, Nijmegen, The Netherlands.

出版信息

Ann Rheum Dis. 1990 Aug;49(8):607-10. doi: 10.1136/ard.49.8.607.

Abstract

Mice with the beige mutation, which are known to be deficient for leucocyte elastase and cathepsin G, were used to investigate the role of neutral proteases in a model for antigen induced arthritis. Surprisingly, it was shown that in this model of arthritis, using methylated bovine serum albumin as an antigen, C57/black/6 'beige' mice (deficient for leucocyte neutral proteases) developed a more severe form of arthritis than the control mice ('black' mice), resulting in a higher degree of tissue damage. The incidence and degree of bone apposition and destruction of articular cartilage at day 21 after induction of arthritis were significantly higher in the beige mice. These findings could not be ascribed to differences in the cellular immune response to methylated bovine serum albumin. Autoradiographic detection of radiolabelled methylated bovine serum albumin suggested that more antigen is retained in the joints of beige mice than in black mice, which might account for the sustained arthritis and the concomitant tissue damage. These findings do not support the contention that leucocyte elastase and cathepsin G contribute to the pathogenesis of joint destruction in this model.

摘要

已知存在米色突变的小鼠缺乏白细胞弹性蛋白酶和组织蛋白酶G,利用这些小鼠在抗原诱导性关节炎模型中研究中性蛋白酶的作用。令人惊讶的是,研究表明,在以甲基化牛血清白蛋白作为抗原的这种关节炎模型中,C57/黑/6“米色”小鼠(缺乏白细胞中性蛋白酶)比对照小鼠(“黑色”小鼠)患更严重形式的关节炎,导致更高程度的组织损伤。在诱导关节炎后第21天,米色小鼠的骨附着和关节软骨破坏的发生率及程度显著更高。这些发现不能归因于对甲基化牛血清白蛋白的细胞免疫反应的差异。放射性标记的甲基化牛血清白蛋白的放射自显影检测表明,米色小鼠关节中保留的抗原比黑色小鼠更多,这可能解释了持续性关节炎及伴随的组织损伤。这些发现不支持白细胞弹性蛋白酶和组织蛋白酶G促成该模型中关节破坏发病机制的观点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3ad8/1004174/c12c74ba75eb/annrheumd00442-0038-a.jpg

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