[ 目的 ]探讨重症肌无力自身抗体分子结构及其在发病机理中的作用 .[方法 ]利用聚合酶链反应从分泌乙酰胆碱受体单克隆抗体A49的杂交瘤细胞株扩增抗体的可变区基因 ,经转化受体菌大肠杆菌DH 5α克隆后 ,进行核苷酸序列分析 .[结果 ]A49的重链可变区基因由小鼠VHNP族基因编码 ,轻链可变区基因由小鼠Vk2组基因编码 ,与致病性乙酰胆碱受体抗体可变区核苷酸序列比较 ,其同源性均在 70 %以下 .[结论 ]A49分子结构与致病性乙酰胆碱受体抗体不同 ,A49诱导大鼠实验性自身免疫性重症肌无力的测定将有助于揭示抗体分子结构与致病性的关系 [Objective] To explore the molecular structure of autoantibody against myasthenia gravis and its role in pathogenesis. [Methods] The variable region gene of antibody was amplified from the hybridoma cell line secreting A49 monoclonal antibody of Ach receptors by polymerase chain reaction , And the nucleotide sequence analysis was performed after the transformed E. coli DH5α was transformed. [Results] The heavy chain variable region gene of A49 was encoded by the mouse VHNP gene and the light chain variable region gene was composed of mouse Vk2 group Compared with the nucleotide sequence of the variable region of pathogenic AChR, the homology was less than 70%. [Conclusion] The A49 molecular structure is different from the pathogenic acetylcholine receptor antibody. The A49 induced rat Determination of experimental autoimmune myasthenia gravis will help reveal the relationship between the molecular structure of the antibody and pathogenicity