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Adjuvant-induced arthritis in rats. Evidence that autoimmunity to homologous collagens types I II IX and XI is not involved in the pathogenesis of arthritis.

机译:佐剂诱发的大鼠关节炎。对IIIIX和XI型同源胶原的自身免疫与关节炎的发病机制无关的证据。

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摘要

We examined the sera of arthritic outbred Wistar and Sprague-Dawley rats and inbred Fisher 344 and Wistar-Lewis rats for autoantibodies to rat type I, II, IX and XI collagens following the induction of arthritis with mycobacteria (MTB). Although many sera collected over an extended time were assayed in addition to acid eluates of arthritic joints, convincing evidence for autoimmunity to collagen could not be demonstrated. Instead, modest non-specific reactions were observed to collagen, irrelevant proteins, and buffer-treated plastic microtitre wells. In contrast, antibodies to purified protein derivative (PPD) were detected in the sera of rats developing adjuvant-induced arthritis, and antibodies to type II collagen, in the sera and joint eluate of rats developing experimental collagen-induced arthritis. Lastly, delayed-type hypersensitivity responses to collagen could not be detected, nor could adjuvant-induced arthritis be attenuated by soluble collagen injected intravenously before challenge with MTB. We conclude that adjuvant-induced arthritis and experimental collagen-induced arthritis are distinct models of rheumatic disease and that autoimmunity to collagen is neither prevalent in adjuvant-induced arthritis nor necessary for its pathogenesis.
机译:我们检查了关节炎近交Wistar和Sprague-Dawley大鼠的血清以及近交Fisher 344和Wistar-Lewis大鼠的血清,以针对分枝杆菌(MTB)诱发关节炎的大鼠I,II,IX和XI型胶原的自身抗体。尽管除了对关节炎关节的酸性洗脱液进行了分析外,还分析了长时间收集的许多血清,但无法证明有针对性的胶原蛋白自身免疫性证据。相反,观察到对胶原蛋白,无关蛋白和缓冲液处理的塑料微量滴定孔的适度非特异性反应。相反,在发展为佐剂诱导的关节炎的大鼠的血清中检测到纯化蛋白衍生物(PPD)的抗体,在发展为实验性胶原诱导的关节炎的大鼠的血清和关节洗脱液中检测到II型胶原的抗体。最后,无法检测到对胶原蛋白的迟发型超敏反应,也不能通过在用MTB攻击之前静脉内注射可溶性胶原蛋白来减轻佐剂诱发的关节炎。我们得出的结论是,佐剂诱导的关节炎和实验性胶原诱导的关节炎是风湿性疾病的独特模型,并且胶原蛋白的自身免疫性在佐剂诱导的关节炎中既不普遍,也不是其发病机理所必需的。

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