Department of Virology, University of Turku, Turku, Finland.
Gene Ther. 2011 Jul;18(7):646-55. doi: 10.1038/gt.2011.4. Epub 2011 Feb 17.
Experimental autoimmune encephalomyelitis (EAE) is an autoimmune inflammation of the central nervous system and is used as the experimental model of multiple sclerosis (MS). The exact mechanism behind the disease is still unknown, but interleukin (IL)-17 expressing T cells are thought to mediate the disease. Toll-like receptors (TLRs) are known to have a role in the innate immune response against pathogens, and several TLRs have also a role in the disease course of EAE. Here, we show that treatment with a herpes simplex virus type 1 vector expressing the Th2 cytokine IL-5 ameliorates EAE and decreases the numbers of infiltrating lymphocytes in the brain. The effect involves downregulation of TLR 2, 3 and 9 mRNA expression and upregulation of type I interferons (IFNs) in brains during onset of disease. The elevated expression of type I IFNs was also observed during recovery.
实验性自身免疫性脑脊髓炎（EAE）是一种中枢神经系统的自身免疫性炎症，被用作多发性硬化症（MS）的实验模型。该疾病的确切机制仍不清楚，但人们认为表达白细胞介素（IL）-17 的 T 细胞介导了该疾病。众所周知，Toll 样受体（TLR）在针对病原体的先天免疫反应中发挥作用，一些 TLR 在 EAE 的疾病过程中也发挥作用。在这里，我们表明，用表达 Th2 细胞因子 IL-5 的单纯疱疹病毒 1 载体进行治疗可以改善 EAE 并减少大脑中浸润的淋巴细胞数量。该作用涉及疾病发作期间大脑中 TLR2、3 和 9 mRNA 表达的下调和 I 型干扰素（IFN）的上调。在恢复期间也观察到 I 型 IFNs 的表达升高。
