Department of Neurosciences NC30, Lerner Research Institute, The Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, Ohio 44195, USA.
J Virol. 2010 Mar;84(6):3111-5. doi: 10.1128/JVI.02373-09. Epub 2009 Dec 30.
Neurotropic coronavirus induces acute encephalomyelitis and demyelination in mice. Infection of BALB/c (H-2(d)) mice expressing a dominant negative gamma interferon (IFN-gamma) receptor specifically in oligodendrocytes was examined to determine the influence of IFN-gamma signaling on pathogenesis. Inhibition of IFN-gamma signaling in oligodendrocytes increased viral load, infection of oligodendrocytes, oligodendrocyte loss, demyelination, and axonal damage resulting in increased mortality. IFN-gamma levels and the inflammatory response were not altered, although the level of tumor necrosis factor (TNF) mRNA was increased. These data indicate that IFN-gamma signaling by oligodendroglia reduces viral replication but affects both demyelination and tissue destruction in a host-specific manner.
神经亲和性冠状病毒诱导小鼠急性脑脊髓炎和脱髓鞘。为了确定 IFN-γ信号对发病机制的影响，检测了在表达显性负 IFN-γ受体的 OL 中特异性表达的 BALB/c（H-2(d)) 小鼠的感染情况。在 OL 中抑制 IFN-γ信号会增加病毒载量、OL 感染、OL 丢失、脱髓鞘和轴突损伤，导致死亡率增加。IFN-γ水平和炎症反应没有改变，尽管 TNF mRNA 水平增加。这些数据表明，OL 的 IFN-γ信号降低了病毒复制，但以宿主特异性的方式影响脱髓鞘和组织破坏。
