Carnegie P R, Mackay I R
Lancet. 1975 Oct 11;2(7937):684-7. doi: 10.1016/s0140-6736(75)90779-5.
A previous hypothesis in which myasthenia gravis was explained by an immune response to acetylcholine receptors has been validated, and is here extended to cell receptors in general. Receptors on target cells, being accessible to circulating trophic hormones or transmitters, must also be accessible to antibodies which compete with the natural mediator for access to the site. To detect anti-receptor antibodies, physiological assay systems would be more sensitive than conventional immunological assays. Autoimmune responses to receptor sites would require a genetic predisposition to failure of immunological tolerance such as occurs in various autoimmune diseases. This hypothesis is supported by recent findings in hyperthyroidism and a type of insulin-resistant diabetes mellitus, and is applicable to other endocrinopathies, diseases in which dysfunction at receptor sites can be postulated, and regulatory functions within the immune system itself.
重症肌无力由针对乙酰胆碱受体的免疫反应所解释这一先前假说已得到验证，并且在此扩展至一般的细胞受体。靶细胞上的受体，由于循环中的营养激素或递质可与之接触，必然也会接触到与天然介质竞争进入该位点的抗体。为检测抗受体抗体，生理学检测系统会比传统免疫学检测更为灵敏。对受体位点的自身免疫反应将需要一种对免疫耐受失败的遗传易感性，就如同在各种自身免疫性疾病中所发生的那样。这一假说得到了甲状腺功能亢进症和一种胰岛素抵抗型糖尿病的最新研究结果的支持，并且适用于其他内分泌疾病、可假定受体位点存在功能障碍的疾病以及免疫系统自身的调节功能。
