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通过对乙酰胆碱受体（ＡＣｈＲ）自身抗体分子结构以及与致病性关系的研究探讨重症肌无力（ＭＧ）及其动物模型——实验性自身免疫性重症肌无力（ＥＡＭＧ）的发病机理。ＡＣｈＲ抗体被动转移至大鼠后诱导出明显的ＥＡＭＧ。全身肌肉ＡＣｈＲ损失率和体重减轻率达４７．２±１５．３％和１３．４±２．２％。这株ＡＣｈＲ抗体的重链可变区基因由小鼠Ｑ５２胚系基因编码，其同源性为９４．８％，将这株抗体的重链和轻链可变区、尤其是互补决定区（ＣＤＲ）的核苷酸和氨基酸序列与其他致病性ＡＣｈＲ抗体比较发现，能诱导ＭＧ和ＥＡＭＧ的致病性ＡＣｈＲ抗体的结构并不是完全一致的。
The pathogenesis of myasthenia gravis (MG) and its animal model, experimental autoimmune myasthenia gravis (EAMG), was explored by studying the molecular structure of AChR autoantibody and its relationship with pathogenicity. Passive AChR antibody transfer to rats induced significant EAMG. Whole body muscle AChR loss rate and weight loss rate of 47.2 ± 15.3% and 13.4 ± 2.2%. The heavy chain variable region gene of this strain of AChR was encoded by mouse Q52 germline gene with a homology of 94.8%. The heavy chain and light chain variable regions of this strain of antibody, especially the complementarity determining region CDR) nucleotide and amino acid sequence compared with other pathogenic AChR antibodies found that the structures of pathogenic AChR antibodies that induce MG and EAMG are not exactly the same.