The class I MHC homologue of human cytomegalovirus inhibits attack by natural killer cells

Hugh T. Reyburn, Ofer Mandelboim, Mar Valés-Gómez, Daniel M. Davis, Laszlo Pazmany and Jack L. Strominger
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Hugh T. Reyburn: Harvard University
Ofer Mandelboim: Harvard University
Mar Valés-Gómez: Harvard University
Daniel M. Davis: Harvard University
Laszlo Pazmany: Harvard University
Jack L. Strominger: Harvard University

Nature, 1997, vol. 386, issue 6624, 514-517

Abstract: 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 hypothesis2). 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.

Date: 1997
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DOI: 10.1038/386514a0

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