从对自身免疫病免疫干扰方面讨论了在抗原存在的情况下通过利用非缺失型抗－ＣＤ４如何诱导无反应性Ｔ细胞。病原Ｔ细胞克隆或杂交瘤识别反应性肽链序列的方法有可能用于识别器官特异性免疫中的Ｔ细胞决定簇。抗原特异疗法最终依赖于肽决定簇。在抗体复合物和ＤＮＡ被特异性Ｂ细胞处理，以及病变的独特型被提呈给具有独特型Ｔ＿Ｈ的情况下，激活对自身抗原特异的Ｂ细胞是可能的。类风湿性关节炎病人具有ＩｇＧ糖基化缺陷。由微生物产生的自身抗原的分子模拟可以通过交叉反应激活自身反应细胞，导致慢性自身免疫状态的建立。 In terms of immune interference with autoimmune diseases, it is discussed how to induce non-reactive T cells by utilizing non-deletion anti-CD4 in the presence of antigen. Pathogenic T cell clones or hybridomas recognize reactive peptide chain sequences as possible for identifying T-cell determinants in organ-specific immunity. Antigen-specific therapies ultimately depend on peptide determinants. It is possible to activate B cells specific for autoantigens in the event that the antibody complex and DNA are treated with specific B cells and the idiotype of the lesion is presented to have the idiotype T_H. Patients with rheumatoid arthritis have IgG glycosylation defects. Molecular modeling of autoantigens produced by microorganisms activates autoreactive cells through cross-reactivity, resulting in the establishment of a chronic autoimmune state.