The University of Southampton
University of Southampton Institutional Repository

The inhibitory receptor NKG2A determines lysis of vaccinia virus-infected autologous targets by NK cells

Brooks, Colin R., Elliott, Tim, Parham, Peter and Khakoo, Salim I. (2006) The inhibitory receptor NKG2A determines lysis of vaccinia virus-infected autologous targets by NK cells Journal of Immunology, 176, (2), pp. 1141-1147. (doi:10.4049/jimmunol.176.2.1141). (PMID:16434388).

Record type: Article


Signals transduced by inhibitory receptors that recognize self-MHC class I molecules prevent NK cells from being activated by autologous healthy target cells. In order for NK cells to be activated upon contact with an infected cell, the balance between the activating and inhibitory signals that regulate NK cell function must be altered in favor of activation. By studying liver-derived NK cells, we show that only a subpopulation of NK cells expressing high levels of the inhibitory receptor NKG2A are able to lyse autologous vaccinia-infected targets, and that this is due to selective down-regulation of HLA-E. These data demonstrate that release from an inhibitory receptor:ligand interaction is one mechanism that permits NK cell recognition of a virally infected target, and that the variegated expression of inhibitory receptors in humans generates a repertoire of NK cells with different antiviral potentials.

Full text not available from this repository.

More information

Published date: 15 January 2006
Keywords: mechanism, hla class-i, dendritic cells, natural-killer-cells, down-regulation, activation, gene-expression, time, human cytomegalovirus, molecules, hepatitis-c virus, t-cells, molecule qa-1(b), antiviral defense, missing self, cells, cell, expression


Local EPrints ID: 62697
ISSN: 0022-1767
PURE UUID: 1a559327-1681-42da-8820-c35dcf2a375f
ORCID for Tim Elliott: ORCID iD

Catalogue record

Date deposited: 05 Sep 2008
Last modified: 17 Jul 2017 14:20

Export record


Download statistics

Downloads from ePrints over the past year. Other digital versions may also be available to download e.g. from the publisher's website.

View more statistics

Atom RSS 1.0 RSS 2.0

Contact ePrints Soton:

ePrints Soton supports OAI 2.0 with a base URL of

This repository has been built using EPrints software, developed at the University of Southampton, but available to everyone to use.

We use cookies to ensure that we give you the best experience on our website. If you continue without changing your settings, we will assume that you are happy to receive cookies on the University of Southampton website.