Granato D, Piguet P F, Fulpius B W
J Neurol Sci. 1980 Sep;47(3):379-83. doi: 10.1016/0022-510x(80)90090-8.
A form of acute experimental autoimmune myasthenia gravis (EAMG) appears within 10 days after immunization of mice with rat acetylcholine receptor (AcChR) in complete adjuvant. This acute phase of EAMG differs from the chronic form reported earlier in the absence of detectable circulating anti-AcChR antibodies and by electrophysiologic signs of neuromuscular blockade which are not reversed by edrophonium injection. This form of acute EAMG occurs similarly in animals whose humoral response has been markedly reduced by pretreatment with cyclophosphamide. These data indicate that the pathogenesis of this acute form might differ from that of chronic EAMG and that it could involve mechanisms of cell-mediated immunity.
在用完全弗氏佐剂中的大鼠乙酰胆碱受体(AcChR)免疫小鼠后10天内,会出现一种急性实验性自身免疫性重症肌无力(EAMG)。EAMG的急性期与先前报道的慢性形式不同,表现为未检测到循环抗AcChR抗体,且注射依酚氯铵后神经肌肉阻滞的电生理体征未得到逆转。这种急性EAMG在经环磷酰胺预处理后体液反应明显降低的动物中也同样会出现。这些数据表明,这种急性形式的发病机制可能与慢性EAMG不同,可能涉及细胞介导的免疫机制。