Stiller C R, Russell A S, Dossetor J B
Ann Intern Med. 1975 Mar;82(3):405-10. doi: 10.7326/0003-4819-82-3-405.
Autoimmune disease may be effected by humoral mechanisms (direct antibody effect or pathogenic antigen-antibody complexes), cell-mediated mechanisms, and possibly complement in the absence of antibody. In view of recent work, self-tolerance can no longer be explained by the clonal selection theory; cells that are capable of recognizing self-antigens and effecting an autoimmune response seem to be present in the normal individual but actively regulated by a process involving antigen-antibody complexes or suppressor T cells. The determination that a clinical state is an autoimmune disease cannot, therefore, be made only on the basis of the presence of autoantibody as this may be part of the normal and active state of immunoregulation of autoimmunity. Indeed, the absence of autoantibody may be the immunodeficient state that allows a full-blown autoimmune disease to occur. In view of this knowledge, the basis for the diagnosis of autoimmune disease and the rationale for treatment based on the objective of inhibiting all immune responses to the autoantigen require re-examination.
自身免疫性疾病可能受体液机制（直接抗体效应或致病性抗原 - 抗体复合物）、细胞介导机制影响，在无抗体时可能还受补体影响。鉴于近期的研究工作，自身耐受性不再能用克隆选择理论来解释；能够识别自身抗原并引发自身免疫反应的细胞似乎存在于正常个体中，但通过涉及抗原 - 抗体复合物或抑制性T细胞的过程受到积极调控。因此，不能仅基于自身抗体的存在来确定一种临床状态为自身免疫性疾病，因为这可能是自身免疫正常和活跃调节状态的一部分。实际上，自身抗体的缺乏可能是允许全面自身免疫性疾病发生的免疫缺陷状态。鉴于这一认识，自身免疫性疾病的诊断依据以及基于抑制对自身抗原的所有免疫反应这一目标的治疗原理需要重新审视。
