Bigazzi P E
Ann N Y Acad Sci. 1986;475:66-80. doi: 10.1111/j.1749-6632.1986.tb20857.x.
It has been hypothesized that autoimmune disease may result from a derangement of the idiotype-anti-idiotype network. However, the evidence in favor of a role of anti-idiotypic immunity in autoimmunity is still scarce. For this reason, we have investigated animal models of autoimmune thyroiditis and glomerulonephritis, addressing the following questions: Are autoimmune responses idiotypically heterogeneous? Are auto-anti-idiotypic antibodies detectable in autoimmunity? Is it possible to demonstrate quantitative or qualitative changes in idiotypic and anti-idiotypic lymphocytes during the course of autoimmune disease? To date, results obtained in our laboratory may be summarized as follows: Cross-reacting idiotypes were present on human and animal autoantibodies; Circulating auto-anti-idiotypic antibodies were not detected in any of the models studied; Changes in idiotypic and anti-idiotypic lymphocytes were observed in animals with autoimmune disease.
有假说认为,自身免疫性疾病可能是由独特型-抗独特型网络紊乱所致。然而,支持抗独特型免疫在自身免疫中起作用的证据仍然不足。因此,我们研究了自身免疫性甲状腺炎和肾小球肾炎的动物模型,探讨以下问题:自身免疫反应在独特型上是否具有异质性?在自身免疫中能否检测到自身抗独特型抗体?在自身免疫性疾病过程中,是否有可能证明独特型和抗独特型淋巴细胞存在数量或质量上的变化?迄今为止,我们实验室获得的结果可总结如下:人和动物自身抗体上存在交叉反应独特型;在所研究的任何模型中均未检测到循环自身抗独特型抗体;在患有自身免疫性疾病的动物中观察到了独特型和抗独特型淋巴细胞的变化。