Holmes Samantha, Friese Manuel A, Siebold Christian, Jones E Yvonne, Bell John, Fugger Lars
Division of Structural Biology, The Henry Wellcome Building for Genomic Medicine, The University of Oxford, Roosevelt Drive, Oxford, OX3 7BN, UK.
Expert Rev Mol Med. 2005 Feb 14;7(3):1-17. doi: 10.1017/S1462399405008914.
Multiple sclerosis (MS) is an autoimmune disease with an important genetic component. The strongest genetic association is with the major histocompatibility complex (MHC) region. Several MHC alleles predispose to the disease, the most prominent of which are certain alleles in the HLA-DR2 haplotype. Functional and structural studies have helped to explain the molecular basis of these associations. Although there is currently no curative treatment for MS, an increased understanding of the disease has aided the design of immunotherapies that act on the immune system more specifically than the longstanding drugs. Many of these therapies work at the antigen-specific level, disrupting the interaction between T-cell receptors and MHC molecules that leads to disease.
多发性硬化症(MS)是一种具有重要遗传成分的自身免疫性疾病。最强的遗传关联与主要组织相容性复合体(MHC)区域有关。几个MHC等位基因易患该疾病,其中最突出的是HLA-DR2单倍型中的某些等位基因。功能和结构研究有助于解释这些关联的分子基础。虽然目前尚无治愈MS的疗法,但对该疾病的进一步了解有助于设计比长期使用的药物更具特异性作用于免疫系统的免疫疗法。许多这些疗法在抗原特异性水平起作用,破坏导致疾病的T细胞受体与MHC分子之间的相互作用。