MOLECULAR MECHANISMS OF AUTOIMMUNE DISEASE IN MAN AND ANIMAL MODELS

在这个项目中，我们试图研究细胞和分子基础。 自身免疫性疾病有两个目的。首先，我们想要确定 致病T细胞的致病作用和抗原特异性 自身免疫性疾病如多发性硬化症、重症肌无力、 胰岛素依赖型糖尿病等。第二，我们想要 确定特异性抗原诱导的细胞凋亡作为一种 治疗这种自身免疫性疾病的方法。为此，我们作出了以下努力 在以下方面取得进展：1)我们成功地建立了 实验性变态反应性脑脊髓炎的绒猴模型 NIH；2)我们发现对绒猴病的抗原治疗导致 改善临床、放射、病理指标； 3)我们优化了一种检测被激活的T细胞的方法 并分泌γ-干扰素以响应髓鞘蛋白抗原和 已经获得了初步证据表明这些细胞在 多发性硬化症患者与正常对照组比较。

In this project we are trying to study the cellular and molecular basis of autoimmune diseases with two purposes. First, we want to establish the pathogenic role and antigen-specificity of T cells that cause autoimmune diseases such as multiple sclerosis, myasthenia gravis, insulin-dependent diabetes, among others. Second, we would like to determine the feasibility of specific antigen-induced apoptosis as a means of treating such autoimmune diseases. To these ends, we have made progress in the following areas: 1) we have successfully established the marmoset model of experimental allergic encephalomyelitis at the NIH; 2) we found that antigen treatment of the marmoset disease leads to amelioration of clinical, radiological, and pathological indices; 3) we have optimized an assay for detecting T cells that are activated and secrete gamma-interferon in response to myelin protein antigens and have obtained preliminary evidence that such cells are increased in multiple sclerosis patients compared to normal controls.