Ji Qingyong, Goverman Joan
Department of Immunology, University of Washington, 1959 NE Pacific Street Seattle, WA 98195-7650, USA.
Ann N Y Acad Sci. 2007 Apr;1103:157-66. doi: 10.1196/annals.1394.017. Epub 2007 Mar 21.
Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system that is believed to have an autoimmune origin. CD4(+) T cells have been well studied for their involvement in the pathogenesis of MS and its animal model, experimental autoimmune encephalomyelitis (EAE). CD8(+) T cells, however, have been overlooked until recently, when more attention has focused on their potential role in pathogenic mechanisms in MS. Here we summarize our work in generating a CD8(+) T cell-mediated EAE model. We discuss immune tolerance mechanisms that regulate CD8(+) T cells specific for myelin basic protein (MBP), and describe initial results regarding triggers of CD8(+) T cell-mediated disease. The availability of CD8(+) T cell-mediated EAE models will help to elucidate the pathogenic roles of CD8(+) T cells in MS, and provide tools for development of novel therapies for MS.
多发性硬化症(MS)是一种中枢神经系统慢性炎症性疾病,被认为具有自身免疫起源。CD4(+) T细胞因其参与MS及其动物模型实验性自身免疫性脑脊髓炎(EAE)的发病机制而得到了充分研究。然而,CD8(+) T细胞直到最近才受到关注,此时更多的注意力集中在它们在MS致病机制中的潜在作用上。在这里,我们总结了我们在建立CD8(+) T细胞介导的EAE模型方面的工作。我们讨论了调节针对髓鞘碱性蛋白(MBP)的CD8(+) T细胞的免疫耐受机制,并描述了关于CD8(+) T细胞介导疾病触发因素的初步结果。CD8(+) T细胞介导的EAE模型的可用性将有助于阐明CD8(+) T细胞在MS中的致病作用,并为开发MS的新疗法提供工具。