Goldman M, Druet P, Gleichmann E
Department of Immunology, Hôpital Erasme, Université Libre de Bruxelles, Belgium.
Immunol Today. 1991 Jul;12(7):223-7. doi: 10.1016/0167-5699(91)90034-Q.
Systemic autoimmune diseases can be induced experimentally in rodents by graft-versus-host or host-versus-graft reactions and by chemicals such as HgCl2, gold salts and D-penicillamine. These models share several features, such as productions of anti-nuclear antibodies, immune glomerulonephritis, MHC class II hyperexpression on B cells, hyper-IgE, increased IL-4 activity and impairment of IL-2 production. This profile of cytokines suggests a central role for TH2-type cells in their pathogenesis. Here, Michel Goldman and colleagues review the data supporting this hypothesis and discuss the possible molecular bases for T-cell activation in chemically-induced systemic autoimmunity.
系统性自身免疫性疾病可通过移植物抗宿主或宿主抗移植物反应以及诸如氯化汞、金盐和青霉胺等化学物质在啮齿动物中实验性诱导产生。这些模型具有若干共同特征,如抗核抗体的产生、免疫性肾小球肾炎、B细胞上MHC II类分子的过度表达、高IgE、IL-4活性增加以及IL-2产生受损。这种细胞因子谱表明TH2型细胞在其发病机制中起核心作用。在此,米歇尔·戈德曼及其同事回顾了支持这一假说的数据,并讨论了化学诱导的系统性自身免疫中T细胞活化的可能分子基础。