Glabinski A R, Tuohy V K, Ransohoff R M
Department of Neurosciences, Cleveland Clinic Foundation, Cleveland, Ohio, USA.
Neuroimmunomodulation. 1998 May-Aug;5(3-4):166-71. doi: 10.1159/000026333.
Experimental autoimmune encephalomyelitis (EAE) is an investigator-initiated disorder that serves as an animal model for the common human demyelinating disease multiple sclerosis. Both diseases are typified by disseminated perivascular and submeningeal cuffs in the central nervous system (CNS). It was shown recently that chemokines are integral to the pathogenesis of EAE. In the present study we analyzed the gene expression of three chemokines, RANTES, MIP-1alpha and GRO-alpha, at the onset of acute EAE, and correlated that expression with the intensity of inflammatory changes in the CNS. We showed that all three chemokines are upregulated simultaneously with symptom onset of acute EAE, and that chemokine expression correlates with the intensity of inflammation in the CNS. This consistent relationship supports the hypothesis that chemokines are relevant to leukocyte accumulation in CNS parenchyma.
实验性自身免疫性脑脊髓炎（EAE）是一种由研究者引发的疾病，可作为常见人类脱髓鞘疾病多发性硬化症的动物模型。这两种疾病的典型特征都是中枢神经系统（CNS）中出现弥漫性血管周围和脑膜下套袖状浸润。最近的研究表明，趋化因子在EAE的发病机制中不可或缺。在本研究中，我们分析了三种趋化因子RANTES、MIP-1α和GRO-α在急性EAE发病时的基因表达，并将该表达与CNS中炎症变化的强度进行关联。我们发现，这三种趋化因子均在急性EAE症状出现时同时上调，且趋化因子表达与CNS中的炎症强度相关。这种一致的关系支持了趋化因子与CNS实质中白细胞积聚相关的假说。
