Trotter J L, Ringel S P, Cook J D, Engel W K, Eldefrawi M E, McFarlin D E
Neurology. 1977 Dec;27(12):1120-4. doi: 10.1212/wnl.27.12.1120.
An indirect immunoperoxidase technique was used to study by light microscopy the binding of serum from experimental autoimmune myasthenia gravis (EAMG) rabbits to junctionally and extrajunctionally located acetylcholine receptors (AChRs) in human and rat muscles. Binding was restricted to junctional AChR. Alpha bungarotoxin (a-BGT) partially blocked the binding of EAMG serum, while myasthenia gravis serum, carbamylcholine, decamethonium, and tubocurarine did not. A radioimmunoassay showed significant binding of antibodies in EAMG sera to 125l AChR. This binding was not inhibited by a-BGT, nor by carbamylcholine, decamethonium, or tubocurarine. Sera from 10 myasthenia gravis patients did not contain antibodies binding to the 125l AChR. We suggest that EAMG in rabbits induced by Torpedo AChR differs serologically from myasthenia gravis in patients, probably owing to antigenic differences between Torpedo and human AChR, and that antigenic differences also exist between junctional and extrajunctional receptors.
采用间接免疫过氧化物酶技术,通过光学显微镜研究实验性自身免疫性重症肌无力(EAMG)兔血清与人及大鼠肌肉中位于接头处和接头外的乙酰胆碱受体(AChR)的结合情况。结合仅限于接头处的AChR。α-银环蛇毒素(α-BGT)部分阻断EAMG血清的结合,而重症肌无力血清、氨甲酰胆碱、十烃季铵和筒箭毒碱则无此作用。放射免疫分析显示EAMG血清中的抗体与125I-AChR有显著结合。这种结合不受α-BGT、氨甲酰胆碱、十烃季铵或筒箭毒碱的抑制。10例重症肌无力患者的血清中未含有与125I-AChR结合的抗体。我们认为,由电鳗AChR诱导的兔EAMG在血清学上与人类患者的重症肌无力不同,这可能是由于电鳗和人类AChR之间的抗原差异所致,并且接头处和接头外受体之间也存在抗原差异。