Richards I, Harrison R, Lunt G G, Bowen J G
J Clin Lab Immunol. 1986 May;20(1):15-21.
Myasthenia gravis is an autoimmune disease in which the autoantigen, the acetylcholine receptor at the neuromuscular junction, is well characterized. As with many other autoimmune diseases, however, the basic cause of immune malfunction is unknown. The autologous mixed lymphocyte reaction (AMLR) involves the proliferation of T lymphocytes when co-cultured with autologous non-T cells and may reflect in vivo mechanisms of immune control. We have measured the AMLR in 22 patients with myasthenia gravis and found the magnitudes of the peak responses to be significantly depressed compared to those of 41 normal healthy controls. Proliferative responses of T cells from myasthenic patients to the mitogens, Concanavalin A and Phytohaemagglutinin-P, were also found to be significantly depressed relative to controls. These abnormal immune cell responses can be, in part, interpreted in terms of defective suppressor cell functions in myasthenia gravis.
重症肌无力是一种自身免疫性疾病,其自身抗原,即神经肌肉接头处的乙酰胆碱受体,已得到充分表征。然而,与许多其他自身免疫性疾病一样,免疫功能异常的根本原因尚不清楚。自体混合淋巴细胞反应(AMLR)涉及T淋巴细胞与自体非T细胞共培养时的增殖,可能反映体内免疫控制机制。我们检测了22例重症肌无力患者的AMLR,发现其峰值反应幅度与41名正常健康对照相比显著降低。重症肌无力患者的T细胞对丝裂原刀豆球蛋白A和植物血凝素-P的增殖反应相对于对照也显著降低。这些异常的免疫细胞反应部分可以用重症肌无力中抑制细胞功能缺陷来解释。