Smirnov V A, Saĭkova L A, Lobzin V S
Biull Eksp Biol Med. 1988 Nov;106(11):549-52.
Single injection of Ig preparations from the myasthenia-patient-blood on C57Bl mice, revealed two phases in the development of the myasthenic syndrome. The first phase started one-two hours after the injection only of the IgM preparation in a dose 2-10 mg. This phase was in progress for two days. The second phase developed during the injection of either the Igm or IgG preparations in a dose 6-10 mg (IgG) of 2-10 mg (IgM). This phase was characterized by the appearance of long myasthenic disorders in two-three week time after the experiment. Some of these mice perished. It was assumed that the absence of strict correlation between the concentration of anti-AChR-IgG antibodies and the gravity of myasthenia is connected with the IgM participation in the pathogenesis of the myasthenia and/or with the appearance of secondary autoantibodies towards the targets which differ from AChR's myoneural synapsis.
给C57Bl小鼠单次注射来自重症肌无力患者血液的免疫球蛋白制剂，揭示了重症肌无力综合征发展的两个阶段。第一阶段在仅注射2 - 10毫克剂量的IgM制剂后一到两小时开始。此阶段持续两天。第二阶段在注射6 - 10毫克（IgG）或2 - 10毫克（IgM）的Igm或IgG制剂期间出现。此阶段的特征是在实验后两到三周出现长期的重症肌无力紊乱。其中一些小鼠死亡。据推测，抗AChR - IgG抗体浓度与重症肌无力严重程度之间缺乏严格相关性与IgM参与重症肌无力发病机制和/或与针对不同于AChR神经肌肉突触靶点的继发性自身抗体的出现有关。
