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The NK cell cytotoxic activity is regulated by both inhibitory and activating NK receptors. Thus, changes in the expression levels and in the affinity or avidity of those receptors will have a major effect on the killing of target cells. In this study, we demonstrate that the binding of NK-inhibitory receptors is enhanced after influenza virus infection. Surprisingly, however, no change in the level of class I MHC protein expression was observed on the surface of the infected cells. The increased binding was general, because it was observed in both the killer cell Ig-like receptor 2 domain long tail 1 and leukocyte Ig-like receptor-1. The increased binding was functional, was not dependent on the interaction with viral hemagglutinin-neuraminidase, was not dependent on the glycosylation site, and was not abolished after mutating the transmembrane or cytosolic portions of the class I MHC proteins. Confocal microscopy experiments showed increased binding of NK receptor-coated beads to infected cells expressing the appropriate class I MHC proteins. In addition, specific cell-free bead aggregates covered with class I MHC proteins were observed only in infected cells. We therefore suggest that the influenza virus use a novel mechanism for the inhibition of NK cell activity. This mechanism probably involves the generation of class I MHC complexes in infected cells that cause increased recognition of NK receptors.

Original publication

DOI

10.4049/jimmunol.171.2.915

Type

Journal article

Journal

Journal of immunology (Baltimore, Md. : 1950)

Publication Date

07/2003

Volume

171

Pages

915 - 923

Addresses

The Lautenberg Center for General and Tumor Immunology, Hebrew University-Hadassah Medical School, Jerusalem, Israel.

Keywords

Killer Cells, Natural, Cells, Cultured, Cell Line, Transformed, COS Cells, Tumor Cells, Cultured, Animals, Humans, Mice, Sendai virus, Influenza A virus, Peptide Fragments, Receptors, Immunologic, Receptors, Virus, Recombinant Fusion Proteins, Antigens, CD, Interleukin-2, HLA-C Antigens, Transfection, Lymphocyte Activation, Microspheres, Species Specificity, Cytotoxicity, Immunologic, Up-Regulation, Protein Binding, Receptors, KIR2DL1