Acha-Orbea H
Ludwig Institute for Cancer Research, Lausanne Branch, Epalinges, Switzerland.
Res Immunol. 1991 Jun-Aug;142(5-6):487-90. doi: 10.1016/0923-2494(91)90053-l.
For many induced and spontaneous autoimmune diseases, a predominant role for T cells in the organ-specific destruction process has been shown. In one of the induced models of autoimmunity, experimental allergic encephalomyelitis (EAE), a very small heterogeneity of T-cell receptor (TcR) molecules is expressed by the pathogenic T cells in both rats and mice. Contrary to induced autoimmune diseases, little is known about the autoantigens recognized by these autoimmune T cells and the heterogeneity of their TcR in spontaneous autoimmune diseases. The aim of this work was to establish a system which allows characterization of relevant autoantigens in spontaneous insulin-dependent diabetes mellitus (IDDM) in non-obese diabetic (NOD) mice. A completely different approach was taken to characterize the gene products of the minor lymphocyte stimulatory (Mls) loci. These gene products are responsible for the clonal elimination or the clonal stimulation of T cells expressing particular TcR V beta genes and therefore could be implicated in induction of autoimmune diseases by oligoclonal T-cell populations. The finding that Mls antigens are encoded by retroviral sequences leads to the hypothesis that viruses could be the inducing agents of autoimmune diseases.
对于许多诱导性和自发性自身免疫性疾病，T细胞在器官特异性破坏过程中已被证明起主要作用。在自身免疫性的诱导模型之一——实验性变应性脑脊髓炎（EAE）中，致病T细胞在大鼠和小鼠中均表达非常小的T细胞受体（TcR）分子异质性。与诱导性自身免疫性疾病相反，对于这些自身免疫性T细胞识别的自身抗原以及它们在自发性自身免疫性疾病中的TcR异质性知之甚少。这项工作的目的是建立一个系统，用于表征非肥胖糖尿病（NOD）小鼠自发性胰岛素依赖型糖尿病（IDDM）中的相关自身抗原。采用了一种完全不同的方法来表征次要淋巴细胞刺激（Mls）位点的基因产物。这些基因产物负责表达特定TcR Vβ基因的T细胞的克隆消除或克隆刺激，因此可能与寡克隆T细胞群体诱导自身免疫性疾病有关。Mls抗原由逆转录病毒序列编码这一发现导致了病毒可能是自身免疫性疾病诱导剂的假说。
