| Literature DB >> 20579746 |
Bo Zhang1, Jigisha Patel, Michelle Croyle, Michael S Diamond, Robyn S Klein.
Abstract
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. (c) 2010 Elsevier B.V. All rights reserved.Entities:
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Year: 2010 PMID： 20579746 PMCID： PMC2910216 DOI： 10.1016/j.jneuroim.2010.05.003
Source DB: PubMed Journal: J Neuroimmunol ISSN： 0165-5728 Impact factor: 3.478