O'Connor K C, Bar-Or A, Hafler D A
Harvard Medical School, Laboratory of Molecular Immunology, Center for Neurologic Diseases, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA.
J Clin Immunol. 2001 Mar;21(2):81-92. doi: 10.1023/a:1011064007686.
Multiple sclerosis (MS) is an inflammatory disease of the central nervous system white matter. The association of the disease with MHC genes, the inflammatory white matter infiltrates, similarities with animal models, and the observation that MS can be treated with immunomodulatory and immunosuppressive therapies support the hypothesis that autoimmunity plays a major role in the disease pathology. Evidence supports activated CD4+ myelin-reactive T cells as major mediators of the disease. In addition, a renewed interest in the possible contribution of B cells to MS immunopathology has been sparked by nonhuman primate and MS pathological studies. This review focuses on the immunopathology of MS, outlining the hypothetical steps of tolerance breakdown and the molecules that play a role in the migration of autoreactive cells to the CNS. Particular focus is given to autoreactive T cells and cytokines as well as B cells and autoantibodies and their role in CNS pathogenesis in MS.
多发性硬化症（MS）是一种中枢神经系统白质的炎性疾病。该疾病与MHC基因的关联、炎性白质浸润、与动物模型的相似性，以及MS可通过免疫调节和免疫抑制疗法进行治疗这一观察结果，均支持自身免疫在疾病病理过程中起主要作用这一假说。有证据表明活化的CD4+髓鞘反应性T细胞是该疾病的主要介导因子。此外，非人类灵长类动物和MS病理学研究引发了人们对B细胞可能在MS免疫病理过程中发挥作用的新兴趣。本综述聚焦于MS的免疫病理学，概述耐受性破坏的假设步骤以及在自身反应性细胞向中枢神经系统迁移中起作用的分子。特别关注自身反应性T细胞和细胞因子，以及B细胞和自身抗体及其在MS中枢神经系统发病机制中的作用。
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