Department of Immunology, University of Washington, Seattle, WA 98195, USA.
Immunol Rev. 2012 Jul;248(1):205-15. doi: 10.1111/j.1600-065X.2012.01126.x.
Multiple sclerosis (MS) is a disease of the central nervous system (CNS) characterized by inflammatory, demyelinating lesions localized in the brain and spinal cord. Experimental autoimmune encephalomyelitis (EAE) is an animal model of MS that is induced by activating myelin-specific T cells and exhibits immune cell infiltrates in the CNS similar to those seen in MS. Both MS and EAE exhibit disease heterogeneity, reflecting variations in clinical course and localization of lesions within the CNS. Collectively, the differences seen in MS and EAE suggest that the brain and spinal cord function as unique microenvironments that respond differently to infiltrating immune cells. This review addresses the roles of the cytokines interferon-γ and interleukin-17 in determining the localization of inflammation to the brain or spinal cord in EAE.
多发性硬化症(MS)是一种中枢神经系统(CNS)疾病,其特征是炎症、脱髓鞘病变局限于大脑和脊髓。实验性自身免疫性脑脊髓炎(EAE)是 MS 的动物模型,通过激活髓鞘特异性 T 细胞诱导,表现出 CNS 中类似于 MS 的免疫细胞浸润。MS 和 EAE 均表现出疾病异质性,反映了临床病程和 CNS 病变定位的变化。总的来说,MS 和 EAE 之间的差异表明大脑和脊髓作为独特的微环境,对浸润的免疫细胞有不同的反应。本综述探讨了细胞因子干扰素-γ和白细胞介素-17 在决定 EAE 中炎症定位到大脑或脊髓中的作用。