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- W27996784 abstract "Abstract Interactions of programmed death 1 (PD-1) with its ligand (PD-L1) contribute to negative regulation of T cell function and dampened anti-viral responses. Following neurotropic coronavirus infection, PD-L1 is prominently upregulated on oligodendroglia, but only modestly on microglia and astrocytes. Concomitant expression of PD-1 on CNS infiltrating virus-specific CD8 T cells implicated PD-1:PD-L1 interactions in contributing to viral persistence in oligodendrocytes. This notion was confirmed by infection of PD-L1 deficient mice (B7-H1-/-). Virus is controlled more rapidly with significantly reduced numbers of infected oligodendrocytes in B7-H1-/- mice compared to wild-type. Accelerated control of infectious virus correlated with enhanced IFN-gamma production, critical to mediate anti-viral function in oligodendroglia. However, the lack of PD-L1 significantly increased disease severity and mortality. High Granzyme B levels and expression of TNF-alpha and iNOS were associated with the enhanced morbidity. Moreover, exacerbated disease in B7-H1-/- mice was coupled with greater axonal damage, while myelin loss was similar. The data demonstrate a significant contribution of PD-L1 in hindering viral clearance in glia cells, while protecting CNS tissue from immune-mediated damage. Supported by NIH NS18146." @default.
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- W27996784 date "2009-04-01" @default.
- W27996784 modified "2023-09-28" @default.
- W27996784 title "PD-L1 expression in the CNS mitigates immune-mediated damage and morbidity at the cost of viral persistence (45.5)" @default.
- W27996784 doi "https://doi.org/10.4049/jimmunol.182.supp.45.5" @default.
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