Abstract
9L glioma cells consistently expressed major histocompatibility complex (MHC) class I but not class II molecules. Herpes simplex type-1 virus (HSV-1) infection significantly reduced the expression of MHC I on the cell surface. Recombinant interferons could enhance the cell-surface expression of MHC I but had no effect on MHC II. This enhancement was partially inhibited by HSV-1 infection. HSV-1 mutants with deletions in ICP4, ICP6, ICP27, ICP47 and UL41 genes do not affect the infection induced inhibition, suggest that a different mechanism may be employed in the inhibition of cell-surface expression of MHC molecules.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Antigens, Surface / analysis
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Antigens, Surface / biosynthesis
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Antigens, Surface / immunology
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Flow Cytometry
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Gene Deletion
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Gene Expression Regulation, Viral / immunology
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Genes, Viral / immunology
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Gliosarcoma / immunology*
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Herpes Simplex / immunology*
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Herpes Simplex / metabolism
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Herpes Simplex / therapy
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Herpesvirus 1, Human / genetics
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Herpesvirus 1, Human / immunology*
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Histocompatibility Antigens Class I / analysis
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Histocompatibility Antigens Class I / biosynthesis*
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Histocompatibility Antigens Class I / immunology
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Histocompatibility Antigens Class II / analysis
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Histocompatibility Antigens Class II / biosynthesis*
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Histocompatibility Antigens Class II / immunology
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Interferon-alpha / pharmacology
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Interferon-beta / pharmacology
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Interferon-gamma / pharmacology
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Rats
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Tumor Cells, Cultured / chemistry
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Tumor Cells, Cultured / immunology
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Tumor Cells, Cultured / metabolism
Substances
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Antigens, Surface
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Histocompatibility Antigens Class I
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Histocompatibility Antigens Class II
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Interferon-alpha
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Interferon-beta
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Interferon-gamma