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• W2899797411 abstract "HSV-1-induced eye disease is a major public health problem. Eye disease is associated closely with immune responses to the virus and is exacerbated by delayed clearance of the primary infection. The immune system relies on antigen-presenting cells of the innate immune system to activate the T cell response. We found that HSV-1 utilizes a robust and finely targeted mechanism of local immune evasion. It downregulates the expression of the costimulatory molecule CD80 but not CD86 on resident dendritic cells irrespective of the presence of anti-HSV-1 antibodies. The effect is mediated by direct binding of HSV-1 ICP22, the product of an immediate early gene of HSV-1, to the promoter of CD80. This immune evasion mechanism dampens the host immune response and, thus, reduces eye disease in ocularly infected mice. Therefore, ICP22 may be a novel inhibitor of CD80 that could be used to modulate the immune response." @default.
• W2899797411 created "2018-11-16" @default.
• W2899797411 creator A5072387109 @default.
• W2899797411 creator A5075884461 @default.
• W2899797411 date "2019-02-01" @default.
• W2899797411 modified "2023-10-15" @default.
• W2899797411 title "Herpes Simplex Virus 1 ICP22 Suppresses CD80 Expression by Murine Dendritic Cells" @default.
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• W2899797411 doi "https://doi.org/10.1128/jvi.01803-18" @default.
• W2899797411 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6340034" @default.
• W2899797411 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30404803" @default.
• W2899797411 hasPublicationYear "2019" @default.
• W2899797411 type Work @default.
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