自1970年以来,有这样一种设想统治着对自身免疫病的研究:正常机体能够产生抗自身抗体,只要这种反应没有被T细胞调节环所控制。许多实验研究和临床研究获得的结果被解释为非特异性T抑制细胞的数目或功能的下降所引起。调节环的瓦解,尤其是抑制性T细胞的缺失被认为是自身免疫病发病的原因。本文拟讨论另一种看待此病的观点,即正常个体没有能与自身抗原起反应的病理性克隆;而其它个体之所以在遗传上易于患自身免疫病是因为他们具有“前禁株” (“pre Since 1970, there is such a hypothesis that dominance in the study of autoimmune diseases: the normal body can produce anti-autoantibodies, as long as this reaction is not controlled by the T-cell regulatory loop. The results obtained in many experimental and clinical studies are explained by the decrease in the number or function of non-specific T-suppressor cells. The disruption of the regulatory loops, particularly the suppression of suppressor T cells, is thought to be responsible for the onset of autoimmune diseases. This article discusses another view of the disease, in which normal individuals do not have pathological colonies that react with their own antigens; other individuals are genetically predisposed to autoimmune disease because of their “pro-ban” "Pre