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为了探讨乙酰胆碱受体（ＡＣｈＲ）抗体阳性重症肌无力患者血浆中的抗体滴度与临床症状之间不平行的原因，作者选用１０例抗体阳性患者作为研究对象，利用ＰｒｏｔｅｉｎＧ层析柱选择性吸附ＩｇＧ的原理从患者血浆中分离ＩｇＧ和非ＩｇＧ两部分，分别观察此两部分对ＴＥ６７１细胞表达的乙酰胆碱受体功能的影响。结果表明，ＩｇＧ部分对ａ－ＢｕＴｘ结合试验具有明显的抑制作用，ＣＰＭ值仅为１５００±２５０（ｎ＝５），非ＩｇＧ部分的抑制作用甚微；ｌｇＧ和非ＩｇＧ部分，两者均对ＡＣｈＲ功能有抑制作用，分别为５８±５％（ｎ＝５）和２５±５％（ｎ＝５）。研究结果提示，非ＩｇＧ部分对ＡＣｈＲ的抑制作用可能是抗体阳性患者抗体滴度与临床症状不平行的原因之一。因此作者认为进一步探讨非ＩｇＧ部分对ＡＣｈＲ的作用机制有助于揭示抗体阳性患者的发病机制。
In order to investigate the reason for the non-parallel antibody titer and clinical symptoms in patients with AChR-positive myasthenia gravis, 10 patients with positive antibodies were selected as the research object, ProteinG was used to selectively adsorb IgG The principle of separation of IgG and non-IgG from the patient’s plasma two parts, respectively, to observe the two parts of TE671 cells expressed acetylcholine receptor function. The results showed that the IgG fraction had a significant inhibitory effect on the a-BuTx binding assay with a CPM value of only 1500 ± 250 (n = 5), with little inhibition of the non-IgG fraction; both lgG and non-IgG fractions, both of AChR Function was inhibited, 58 ± 5% (n = 5) and 25 ± 5% (n = 5), respectively. The results suggest that non-IgG part of the AChR inhibition may be antibody-positive antibody titer and clinical symptoms of one of the reasons. Therefore, the authors believe that further exploration of the non-IgG part of the AChR mechanism may help reveal the pathogenesis of antibody-positive patients.