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小鼠实验性自身免疫性重症肌无力中临床疾病与抗体滴度、增殖反应及神经生理学的关系。

The relation of clinical disease to antibody titre, proliferative response and neurophysiology in murine experimental autoimmune myasthenia gravis.

作者信息

Pachner A R, Kantor F S

出版信息

Clin Exp Immunol. 1983 Mar;51(3):543-50.

Abstract

Murine myasthenia is a relatively faithful model of the human disease. We studied anti-AChR antibody titres, lymphocyte proliferative response to AChR, characteristic electromyographic (EMG) abnormalities and muscle strength at weekly intervals after immunization of C57B16J mice with Torpedo AChR. The boosting immunization at 1 month after the primary immunization resulted in a progressive increase of anti-AChR IgG antibodies, but caused a marked drop in the proliferative response. Although characteristic EMG abnormalities occurred in nearly all immunized mice, clinical disease appeared very late or not at all. These data parallel findings in human myasthenia.

摘要

小鼠重症肌无力是人类疾病的一种较为可靠的模型。在用电鳐乙酰胆碱受体(Torpedo AChR)免疫C57B16J小鼠后,我们每周检测抗乙酰胆碱受体(AChR)抗体滴度、淋巴细胞对AChR的增殖反应、特征性肌电图(EMG)异常以及肌肉力量。初次免疫后1个月进行加强免疫导致抗AChR IgG抗体逐渐增加,但增殖反应显著下降。尽管几乎所有免疫小鼠都出现了特征性EMG异常,但临床疾病出现得非常晚或根本未出现。这些数据与人类重症肌无力的研究结果相似。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f4ee/1536805/a7e2a246c776/clinexpimmunol00162-0136-a.jpg

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