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- W4313374636 abstract "Abstract West Nile Virus (WNV) is a leading cause of mosquito-borne neuroinvasive disease in the US. Following infection, WNV can cause neuronal injury and disease. Previous studies have shown that the proper activation of virus-specific T cells results in protection from WNV infection and any associated disease. Dendritic cells (DCs) are often defined as pivotal inducers of immunity due to their role in activating immune defense mechanisms against invading pathogens. XCR1, a chemokine receptor expressed predominantly by a subset of DCs, has been shown to be essential in cross-presenting antigen and in activating anti-viral immunity. However, DCs are not readily present within the CNS and it remains unknown how DCs are recruited to the CNS during WNV encephalitis to fully activate antiviral immunity. XCL1, the ligand for XCR1, is expressed by activated T cells, DCs, macrophages, and NK cells. We hypothesize that following WNV infection, virus-specific T cells within the CNS produce XCL1 in order to recruit and stabilize their interaction with XCR1+ DCs thus ensuring their proper activation and subsequent protection against WNV encephalitis. Here we demonstrate that mice lacking XCR1+ DCs are more susceptible to WNV encephalitis, display increased neuronal cell death, as well as increased viral burden compared to control animals. In addition, in the absence of XCR1+ DCs, WNV-infected animals displayed decreased parenchymal localization of T cells within the brain compared to controls. These data indicate that XCL1-XCR1 interactions are crucial in the development of efficient anti-viral immunity. The knowledge gained from this work may then be applicable to other viral diseases of the CNS." @default.
- W4313374636 created "2023-01-06" @default.
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- W4313374636 date "2020-05-01" @default.
- W4313374636 modified "2023-09-26" @default.
- W4313374636 title "T cell-derived XCL1 induces protective immunity against West Nile virus within the CNS" @default.
- W4313374636 doi "https://doi.org/10.4049/jimmunol.204.supp.248.1" @default.
- W4313374636 hasPublicationYear "2020" @default.
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