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首页> 外文期刊>Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology >TNF-alpha-dependent regulation of CXCR3 expression modulates neuronal survival during West Nile virus encephalitis.
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TNF-alpha-dependent regulation of CXCR3 expression modulates neuronal survival during West Nile virus encephalitis.

机译：TNF-α依赖的CXCR3表达调节在西尼罗河病毒性脑炎期间调节神经元存活。

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摘要

The chemokine CXCL10 exerts antiviral effects within the central nervous system (CNS) through the recruitment of virus-specific T cells. However, elevated levels of CXCL10 may induce neuronal apoptosis given its receptor, CXCR3, is expressed by neurons. Using a murine model of West Nile virus (WNV) encephalitis, we determined that WNV-infected neurons express TNF-alpha, which down-regulates neuronal CXCR3 expression via signaling through TNFR1. Down-regulation of neuronal CXCR3 decreased CXCL10-mediated calcium transients and delayed Caspase 3 activation. Loss of CXCR3 activation, via CXCR3-deficiency or pretreatment with TNF-alpha prevented neuronal apoptosis during in vitro WNV infection. These results suggest that neuronal TNF-alpha expression during WNV encephalitis may be an adaptive response to diminish CXCL10-induced death.
机译：趋化因子CXCL10通过募集病毒特异性T细胞在中枢神经系统（CNS）中发挥抗病毒作用。但是，鉴于其受体CXCR3由神经元表达，CXCL10水平升高可能会诱导神经元凋亡。使用西尼罗河病毒（WNV）脑炎的小鼠模型，我们确定WNV感染的神经元表达TNF-α，它通过通过TNFR1的信号下调神经元CXCR3的表达。神经元CXCR3的下调减少了CXCL10介导的钙瞬变和延迟的Caspase 3激活。通过CXCR3缺乏或使用TNF-α预处理，CXCR3激活的丧失阻止了体外WNV感染期间的神经元凋亡。这些结果表明在WNV脑炎期间神经元TNF-α表达可能是减少CXCL10诱导的死亡的适应性反应。

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