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一、发病机制现今认为重症肌无力(MG)是随意肌的自体免疫性突触后膜乙酰胆碱受体(AchR)病。即由于血中的抗 AchR 抗体对受体的封闭使它不能与 Ach 有效的结合;抗体与受体结合的复合物在补体 C_3参与之下可以溶解受体;杀伤 T 细胞及淋巴因子可以直接破坏受体,这样使受体的数目减少,使突触后膜的形态改变。辅助 T 细胞可以促进 B 细胞合成抗 AchR 抗体。这种抗体不仅在胸腺外合成,而且可在胸腺内合成。现今已发现 T 淋巴细胞之所以能被致敏,是因为患者的胸腺内存有抗原(带有 AchR 的肌样细胞)。此外
First, the pathogenesis Now that myasthenia gravis (MG) is a voluntary muscle autoimmune postsynaptic membrane acetylcholine receptor (AchR) disease. That is, the blocking of the receptor by the anti-AchR antibody in blood makes it unable to effectively bind with Ach; the antibody-receptor complex can dissolve the receptor under the participation of complement C_3; the killing of T cells and lymphokines can directly destroy Receptors, so that the number of receptors to reduce the morphological changes of the postsynaptic membrane. Helper T cells can promote B cell synthesis of anti-AchR antibodies. This antibody is synthesized not only outside the thymus, but also inside the thymus. T lymphocytes have now been found to be sensitized because of the presence of antigen (myoid-like cells with AchR) in the patient’s thymus. In addition