Abstract
Recognition and destruction of virus-infected cells by class I major histocompatibility complex (MHC) restricted cytotoxic T lymphocytes (CTL) is a central part of the immune system's attempts to control and eliminate virus infection. It is therefore not surprising that many viruses have evolved strategies to interfere with the processing and presentation of peptide antigen on class I MHC molecules (reviewed in ref. 1). These mechanisms act to prevent or reduce expression of MHC molecules at the cell surface. However, many natural killer (NK) cells are able to recognize and destroy host cells that no longer express class I MHC molecules (the 'missing self' hypothesis). Thus, any virus-infected cell that has lost cell-surface expression of MHC class I to avoid CTL attack should become susceptible to NK-cell-mediated destruction. We describe here the first example, to our knowledge, of a viral strategy to evade immune surveillance by NK cells.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Antigens, CD / metabolism
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Cell Line
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Cytomegalovirus / immunology*
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Cytomegalovirus / metabolism
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Glycoside Hydrolases / antagonists & inhibitors
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Glycoside Hydrolases / metabolism
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Glycosylation
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Histocompatibility Antigens Class I / immunology*
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Humans
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Killer Cells, Natural / immunology*
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Lectins / metabolism
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Lectins, C-Type*
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Membrane Glycoproteins / metabolism
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NK Cell Lectin-Like Receptor Subfamily D
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Receptors, Virus / metabolism
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Recombinant Proteins / immunology
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Sequence Homology, Amino Acid
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Transfection
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Viral Proteins / genetics
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Viral Proteins / immunology*
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beta 2-Microglobulin / genetics
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beta 2-Microglobulin / immunology*
Substances
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Antigens, CD
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Histocompatibility Antigens Class I
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Lectins
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Lectins, C-Type
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Membrane Glycoproteins
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NK Cell Lectin-Like Receptor Subfamily D
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Receptors, Virus
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Recombinant Proteins
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Viral Proteins
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beta 2-Microglobulin
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Glycoside Hydrolases