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针对II型胶原蛋白的自身免疫反应——一种关节炎实验模型

Autoimmunity to type II collagen an experimental model of arthritis.

作者信息

Trentham D E, Townes A S, Kang A H

出版信息

J Exp Med. 1977 Sep 1;146(3):857-68. doi: 10.1084/jem.146.3.857.

Abstract

We have found that intradermal injection of native type II collagen extracted from human, chick or rat cartilage induces an inflammatory arthritis in approximately 40% of rats of several strains whether complete Freund's adjuvant or incomplete Freund's adjuvant is used. Type I or III collagen extracted from skin, cartilage proteoglycans and alpha1(II) chains were incapable of eliciting arthritis, as was type II collagen injected without adjuvant. The disease is a chronic proliferative synovitis, resembling adjuvant arthritis in rats and rheumatoid arthritis in humans. Native type II co-lagen modified by limited pepsin digestion still produces arthritis, suggesting that type-specific determinants residing in the helical region of the molecule are responsible for the induction of disease. Since homologous type II collagen emulsified in oil without bacterial preparations regularly causes the disease, this new animal model of arthritis represents a unique example of experimentally-inducible autoimmunity to a tissue component.

摘要

我们发现,无论使用完全弗氏佐剂还是不完全弗氏佐剂,皮内注射从人、鸡或大鼠软骨中提取的天然II型胶原蛋白,在几种品系的大约40%的大鼠中会诱发炎性关节炎。从皮肤、软骨蛋白聚糖和α1(II)链中提取的I型或III型胶原蛋白不能引发关节炎,未加佐剂注射的II型胶原蛋白也是如此。该疾病是一种慢性增殖性滑膜炎,类似于大鼠的佐剂性关节炎和人类的类风湿性关节炎。经有限胃蛋白酶消化修饰的天然II型胶原蛋白仍会引发关节炎,这表明分子螺旋区域中存在的型特异性决定簇是诱发疾病的原因。由于在没有细菌制剂的情况下在油中乳化的同源II型胶原蛋白经常会引发该疾病,这种新的关节炎动物模型代表了对组织成分进行实验诱导性自身免疫的独特例子。

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