Institut National de la Santé et de la Recherche Médicale, Unité 563, Toulouse, France.
Cell Mol Life Sci. 2010 Dec;67(23):4011-34. doi: 10.1007/s00018-010-0481-9. Epub 2010 Aug 17.
Multiple sclerosis (MS) is an inflammatory demyelinating disease affecting the central nervous system (CNS) and a frequent cause of neurological disability in young adults. Multifocal inflammatory lesions in the CNS white matter, demyelination, oligodendrocyte loss, axonal damage, as well as astrogliosis represent the histological hallmarks of the disease. These pathological features of MS can be mimicked, at least in part, using animal models. This review discusses the current concepts of the immune effector mechanisms driving CNS demyelination in murine models. It highlights the fundamental contribution of transgenesis in identifying the mediators and mechanisms involved in the pathophysiology of MS models.
多发性硬化症(MS)是一种影响中枢神经系统(CNS)的炎症性脱髓鞘疾病,也是年轻人中常见的神经功能障碍原因。CNS 白质中的多灶性炎症性病变、脱髓鞘、少突胶质细胞丢失、轴突损伤以及星形胶质细胞增生代表了该疾病的组织学特征。这些 MS 的病理学特征至少在一定程度上可以通过动物模型来模拟。本综述讨论了当前关于在小鼠模型中驱动 CNS 脱髓鞘的免疫效应机制的概念。它强调了转基因在确定 MS 模型的病理生理学中涉及的介质和机制方面的基本贡献。