Verschuuren J J, Graus Y M, Theunissen R O, Yamamoto T, Vincent A, van Breda Vriesman P J, De Baets M H
Department of Immunology, University of Limburg, Maastricht, Netherlands.
J Neuroimmunol. 1992 Feb;36(2-3):117-25. doi: 10.1016/0165-5728(92)90043-k.
In experimental autoimmune myasthenia gravis anti-rat nicotinic acetylcholine receptor (AChR) antibody titers correlated significantly with the AChR-antibody complexes found in muscle. It was shown that at least a large part of the AChR-antibody complexes are formed in vitro, which can be prevented by washing of the muscle homogenate. Using a modified assay, no differences in AChR-antibody complexes could be detected between rats with and without symptoms of experimental autoimmune myasthenia gravis. Also no difference in AChR loss nor in inhibition of alpha-bungarotoxin binding to AChR was found between these groups of rats. However, a significant difference in the reduction of AChR function was found, using an assay measuring agonist-induced 22Na+ flux into the TE671 cell line.
在实验性自身免疫性重症肌无力中,抗大鼠烟碱型乙酰胆碱受体(AChR)抗体滴度与肌肉中发现的AChR抗体复合物显著相关。结果表明,至少大部分AChR抗体复合物是在体外形成的,这可以通过洗涤肌肉匀浆来预防。使用改良的检测方法,在有和没有实验性自身免疫性重症肌无力症状的大鼠之间未检测到AChR抗体复合物的差异。在这些大鼠组之间,AChR丢失以及α-银环蛇毒素与AChR结合的抑制也没有差异。然而,使用测量激动剂诱导的22Na+流入TE671细胞系的检测方法,发现AChR功能降低存在显著差异。