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使用非离子型嵌段共聚物作为佐剂,通过乙酰胆碱受体诱导实验性自身免疫性重症肌无力。

Induction of experimental autoimmune myasthenia gravis with acetylcholine receptors using a nonionic block copolymer as adjuvant.

作者信息

Shenoy M, Christadoss P

机构信息

Department of Microbiology, University of Texas Medical Branch, Galveston 77550.

出版信息

Immunol Invest. 1993 Jun;22(4):267-82. doi: 10.3109/08820139309063408.

Abstract

To induce autoimmune diseases in animals, the auto-antigen has to be emulsified in adjuvants (e.g., complete Freund's adjuvant) containing microbial products such as Mycobacterium tuberculosis. But these powerful immunoadjuvants are not without undesirable immune response to the microbial proteins and induction of adjuvant arthritis, which could interfere with the antigen specific autoimmune response to be tested. This study was performed to evaluate the requirement of microbial products in the induction of experimental autoimmune diseases, and to identify an adjuvant without unwanted immune responses. C57BL/6 mice were inoculated with Torpedo acetylcholine receptors (T-AChR) emulsified in Titermax (TM), an adjuvant containing nonionic block copolymer and no microbial products, and evaluated for experimental autoimmune myasthenia gravis (EAMG) susceptibility. Mice immunized with T-AChR in TM demonstrated characteristic myasthenic muscle weakness with electrophysiological defect, elevated serum anti-AChR antibodies, and muscle AChR loss. None of the mice that received TM alone had muscle weakness, serum anti-AChR antibodies or muscle AChR loss. The data imply that microbial products are not critical in the induction of autoimmune diseases like myasthenia gravis in mice. Further, nonionic block copolymer could be an ideal adjuvant in the induction of autoimmune diseases in animals.

摘要

为了在动物中诱导自身免疫性疾病,自身抗原必须在含有微生物产物(如结核分枝杆菌)的佐剂(如完全弗氏佐剂)中乳化。但这些强大的免疫佐剂并非没有对微生物蛋白产生不良免疫反应以及诱导佐剂性关节炎的问题,这可能会干扰待测试的抗原特异性自身免疫反应。本研究旨在评估微生物产物在诱导实验性自身免疫性疾病中的必要性,并确定一种无不良免疫反应的佐剂。将用TiterMax(TM)乳化的电鳐乙酰胆碱受体(T-AChR)接种C57BL/6小鼠,TM是一种含有非离子嵌段共聚物且无微生物产物的佐剂,并评估其对实验性自身免疫性重症肌无力(EAMG)的易感性。用TM中的T-AChR免疫的小鼠表现出具有电生理缺陷的典型肌无力,血清抗AChR抗体升高,以及肌肉AChR丢失。单独接受TM的小鼠均无肌无力、血清抗AChR抗体或肌肉AChR丢失。数据表明微生物产物在诱导小鼠重症肌无力等自身免疫性疾病中并非至关重要。此外,非离子嵌段共聚物可能是诱导动物自身免疫性疾病的理想佐剂。

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