Pender Michael P, Greer Judith M
Neuroimmunology Research Centre, Clinical Sciences Building, Royal Brisbane and Womens Hospital, Herston, Queensland 4029, Australia.
Curr Allergy Asthma Rep. 2007 Jul;7(4):285-92. doi: 10.1007/s11882-007-0043-x.
Multiple sclerosis (MS) is an autoimmune disease of the central nervous system (CNS) leading to demyelination, axonal damage, and progressive neurologic disability. The development of MS is influenced by environmental factors, particularly the Epstein-Barr virus (EBV), and genetic factors, which include specific HLA types, particularly DRB11501-DQA10102-DQB1*0602, and a predisposition to autoimmunity in general. MS patients have increased circulating T-cell and antibody reactivity to myelin proteins and gangliosides. It is proposed that the role of EBV is to infect autoreactive B cells that then seed the CNS and promote the survival of autoreactive T cells there. It is also proposed that the clinical attacks of relapsing-remitting MS are orchestrated by myelin-reactive T cells entering the white matter of the CNS from the blood, and that the progressive disability in primary and secondary progressive MS is caused by the action of autoantibodies produced in the CNS by -meningeal lymphoid follicles with germinal centers.
多发性硬化症（MS）是一种中枢神经系统（CNS）的自身免疫性疾病，可导致脱髓鞘、轴突损伤和进行性神经功能残疾。MS的发生受环境因素影响，尤其是爱泼斯坦-巴尔病毒（EBV），以及遗传因素，其中包括特定的人类白细胞抗原（HLA）类型，特别是DRB11501-DQA10102-DQB1*0602，以及一般的自身免疫易感性。MS患者对髓鞘蛋白和神经节苷脂的循环T细胞和抗体反应性增加。有人提出，EBV的作用是感染自身反应性B细胞，这些细胞随后进入中枢神经系统并促进那里自身反应性T细胞的存活。也有人提出，复发缓解型MS的临床发作是由髓鞘反应性T细胞从血液进入中枢神经系统白质所引发的，而原发性和继发性进展型MS的进行性残疾是由中枢神经系统中具有生发中心的脑膜淋巴滤泡产生的自身抗体的作用所导致的。
