Wekerle H
Max-Planck-Institut for Psychiatry, Martinsried, Germany.
Curr Opin Neurobiol. 1993 Oct;3(5):779-84. doi: 10.1016/0959-4388(93)90153-p.
Experimental autoimmune encephalomyelitis models are used to analyze the generation and organization of the myelin-specific autoimmune repertoire, and potential immunoregulatory loops preventing spontaneous activation of encephalitogenic T cells. These lymphocytes are profoundly modulated by infectious agents, which may trigger, or more commonly, prevent experimental autoimmune encephalomyelitis. The development and resolution of the pathogenic central nervous system infiltrations is controlled by locally produced cytokines that cause recruitment of infiltrate cells, and their disappearance. Several of the new findings seem now to be applicable for therapeutic strategies, especially with the aim of interfering with immunospecific recognition steps involved in disease generation.
实验性自身免疫性脑脊髓炎模型用于分析髓鞘特异性自身免疫库的产生和组织,以及防止致脑炎性T细胞自发激活的潜在免疫调节回路。这些淋巴细胞受到感染因子的深刻调节,感染因子可能引发实验性自身免疫性脑脊髓炎,或者更常见的是预防该疾病。致病性中枢神经系统浸润的发展和消退由局部产生的细胞因子控制,这些细胞因子导致浸润细胞的募集及其消失。现在一些新发现似乎适用于治疗策略,特别是旨在干扰疾病产生过程中涉及的免疫特异性识别步骤。