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- W2035771736 abstract "ABSTRACT HLA-G is a nonclassical human major histocompatibility complex class I molecule. It may promote tolerance, leading to acceptance of the semiallogeneic fetus and tumor immune escape. We show here that two viruses—herpes simplex virus type 1 (HSV-1), a neuronotropic virus inducing acute infection and neuron latency; and rabies virus (RABV), a neuronotropic virus triggering acute neuron infection—upregulate the neuronal expression of several HLA-G isoforms, including HLA-G1 and HLA-G5, the two main biologically active isoforms. RABV induces mostly HLA-G1, and HSV-1 induces mostly HLA-G3 and HLA-G5. HLA-G expression is upregulated in infected cells and neighboring uninfected cells. Soluble mediators, such as beta interferon (IFN-β) and IFN-γ, upregulate HLA-G expression in uninfected cells. The membrane-bound HLA-G1 isoform was detected on the surface of cultured RABV-infected neurons but not on the surface of HSV-1-infected cells. Thus, neuronotropic viruses that escape the host immune response totally (RABV) or partially (HSV-1) regulate HLA-G expression on human neuronal cells differentially. HLA-G may therefore be involved in the escape of certain viruses from the immune response in the nervous system." @default.
- W2035771736 created "2016-06-24" @default.
- W2035771736 creator A5011706989 @default.
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- W2035771736 date "2005-12-15" @default.
- W2035771736 modified "2023-10-18" @default.
- W2035771736 title "Modulation of HLA-G Expression in Human Neural Cells after Neurotropic Viral Infections" @default.
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- W2035771736 doi "https://doi.org/10.1128/jvi.79.24.15226-15237.2005" @default.
- W2035771736 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1316015" @default.
- W2035771736 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/16306594" @default.
- W2035771736 hasPublicationYear "2005" @default.
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