6533b7d3fe1ef96bd1260177
RESEARCH PRODUCT
Inhibition of the NKp30 activating receptor by pp65 of human cytomegalovirus.
Jacob H. HannaGil KatzEfrat NahariTsufit Gonen-grossAlik HonigmanTal I. ArnonAngel PorgadorGal MarkelRoi GazitHagit AchdoutOfer LeviBodo PlachterOfer MandelboimNivin SalehDana G. WolfDror Mevorachsubject
Cytotoxicity ImmunologicHuman cytomegalovirusViral proteinvirusesImmunologyCytomegalovirusReceptors Cell SurfaceBiologymedicine.disease_causeNatural killer cellViral Matrix ProteinsMiceImmune systemmedicineAnimalsHumansImmunology and AllergyReceptors ImmunologicCytotoxicityReceptorCells CulturedMembrane GlycoproteinsNatural Cytotoxicity Triggering Receptor 3virus diseasesPhosphoproteinsmedicine.diseaseVirologyImmunoglobulin Fc FragmentsCell biologyKiller Cells NaturalNatural Cytotoxicity Triggering Receptor 3Kineticsmedicine.anatomical_structureGene Expression RegulationIntracellularProtein Bindingdescription
Human cytomegalovirus, a chief pathogen in immunocompromised people, can persist in a healthy immunocompetent host throughout life without being eliminated by the immune system. Here we show that pp65, the main tegument protein of human cytomegalovirus, inhibited natural killer cell cytotoxicity by an interaction with the activating receptor NKp30. This interaction was direct and specific, leading to dissociation of the linked CD3zeta from NKp30 and, consequently, to reduced killing. Thus, pp65 is a ligand for the NKp30 receptor and demonstrates a unique mechanism by which an intracellular viral protein causes general suppression of natural killer cell cytotoxicity by specific interaction with an activating receptor.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2005-04-10 | Nature immunology |