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乙酰胆碱受体（ＡＣｈＲ）抗体在重症肌无力（ＭＧ）和实验性自身免疫性重症肌无力（ＥＡＭＧ）患者体内可诱导ＡＣｈＲ丢失和肌力减退。通过对小鼠抗电鳐电器官的ＡＣｈＲ单抗Ａ７的致病性测定和可变区基因克隆与序列分析， 探讨致病性抗体介导的ＭＧ和ＥＡＭＧ的发病机制。Ａ７被动注射大鼠后可诱导出严重的ＥＡＭＧ，ＡＣｈＲ损失串达３８．４％±７．２％。Ａ７的Ｈ链Ｖ区由小鼠ＰＣ７１８３胚系基因编码与Ｄ和ＪＨ４连接，与ＤＦＬ１６．２胚系Ｖ_Ｈ基因具有９３．７％的同源性。Ｌ链Ｖ区由小鼠Ｖ_Ｋ３组基因编码，与Ｊｋ２连接，与Ｖｋ２１Ｅ胚系基因具有９８．１％的同源性。
Acetylcholine receptor (AChR) antibodies induce AChR loss and muscle weakness in patients with myasthenia gravis (MG) and experimental autoimmune myasthenia gravis (EAMG). Through pathogenicity test and variable region gene cloning and sequence analysis of AChR McAb A7 in mice, the pathogenic antibody-mediated pathogenesis of MG and EAMG was explored. Severe EAMG was induced after passive injection of A7 in rats, with an AChR loss of 38.4% ± 7.2%. The H chain V region of A7 was linked to D and JH4 by the mouse PC7183 germline gene and has 93.7% homology with DFL16.2 germline V_H gene. The L chain V region was encoded by the mouse V_K3 gene and linked to Jk2 with 98.1% homology with the Vk21E germline gene.