Luppi P, Rossiello M R, Faas S, Trucco M
Department of Pediatrics, Rangos Research Center, Children's Hospital of Pittsburgh, University of Pittsburg, School of Medicine, PA 15213, USA.
J Mol Med (Berl). 1995 Aug;73(8):381-93. doi: 10.1007/BF00240137.
Autoimmune diseases result from the breakdown of "self" tolerance. Environmental factors appear to be responsible for triggering this errant immune response, directed against self-tissue determinants, only when a susceptible genetic background is present in an individual. Autoimmune diseases, normally characterized by their association with certain HLA alleles, also share other features: the presence of autoantibodies, autoreactive T lymphocytes, and an intermittent clinical course of exacerbations and remissions. In cases of organ-specific diseases, as well as in cases of multi-system autoimmune diseases, viruses are increasingly implicated as such environmental triggers. Current molecular biology techniques have permitted a fine dissection of the genetic background of susceptible individuals and have enabled a more complete characterization of the immunocompetent cells involved in this autoaggression. Molecular approaches will soon allow us to pinpoint the characteristics of the environmental stimuli, so that protective strategies could be formulated to spare susceptible individuals from their ill effects.
自身免疫性疾病是由“自身”耐受性的破坏引起的。环境因素似乎是引发这种针对自身组织决定簇的错误免疫反应的原因，而且只有当个体存在易感基因背景时才会如此。自身免疫性疾病通常以与某些人类白细胞抗原（HLA）等位基因相关为特征，它们还具有其他共同特征：存在自身抗体、自身反应性T淋巴细胞，以及病情加重和缓解交替出现的间歇性临床病程。在器官特异性疾病以及多系统自身免疫性疾病中，病毒越来越多地被认为是这类环境触发因素。当前的分子生物学技术已能够精细剖析易感个体的基因背景，并能更全面地描述参与这种自身攻击的免疫活性细胞的特征。分子生物学方法很快将使我们能够确定环境刺激的特征，从而制定出保护策略，使易感个体免受其不良影响。
