Enhanced recognition of human NK receptors after influenza virus infection
| Autor: | Eli Kedar, Tsufit Gonen-Gross, Gil Katz, Tal I. Arnon, Hagit Achdout, Gal Markel, Niva Lieberman, Ofer Mandelboim, Roi Gazit, Aviva Joseph |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2003 |
| Předmět: |
Cytotoxicity
Immunologic Virus genetics Recombinant Fusion Proteins Immunology Leukocyte Immunoglobulin-like Receptor B1 HLA-C Antigens Major histocompatibility complex Lymphocyte Activation Transfection Sendai virus Mice Antigen KIR2DL1 Species Specificity Antigens CD MHC class I Tumor Cells Cultured Immunology and Allergy Cytotoxic T cell Animals Humans Receptors Immunologic Receptor Cells Cultured Cell Line Transformed biology Molecular biology Microspheres Peptide Fragments Up-Regulation Killer Cells Natural Influenza A virus COS Cells Receptors KIR2DL1 biology.protein Interleukin-2 Receptors Virus Protein Binding |
| Zdroj: | Journal of immunology (Baltimore, Md. : 1950). 171(2) |
| ISSN: | 1550-6606 0022-1767 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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