Simultaneous avoidance of CD8+ and NK cell-mediated virus control by the MCMV m152 gene product (CROSBI ID 493710)
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Podaci o odgovornosti
Krmpotić, Astrid ; Bubić, Ivan ; Hengel, Hartmut ; Scalzo, Anthony ; Koszinowski, Ulrich ; Jonjić, Stipan
engleski
Simultaneous avoidance of CD8+ and NK cell-mediated virus control by the MCMV m152 gene product
The MCMV glycoprotein gp40, encoded by the m152 gene retains MHC class-I complexes in the ERGIC/cis-Golgi compartment, allowing the virus to evade control by CD8+ T lymphocytes in vivo (Krmpotic et al., J Exp Med 1999 190:1285). Given that cell surface class I molecules interact with inhibitory receptors to avoid NK cell attack, down modulation of MHC-I molecules may increase MCMV susceptibility to NK cells. In spite of this, we found that gp40 severely inhibits NK cell-mediated virus control in vivo. This effect is mouse strain dependent but independent of Cmv1, a locus which restricts early MCMV replication in the spleen through the action of NK cells. In mouse strains sensitive to the gp40-mediated effect (e.g. BALB/c) the NK cell response is strongly attenuated by the expression of m152, while in resistant strains, (e.g. B6) replication of both the m152 deletion mutant and the m152 revertant virus is efficiently controlled by NK cells. Transfer studies of MCMV infected cells from resistant into sensitive strains revealed that both NK receptors as well as ligands present on NK stimulator cells determine the m152/gp40 phenotype. In our study, we made use of intra&#8211 ; natural killer complex (NKC) recombinant BALBc/B6 and congenic mouse strains for mapping the loci encompassing gp40-sensitive NK cell receptor(s) on mouse chromosome 6.
MCMV; m152; NK cells; NKG2D
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Podaci o prilogu
56-x.
2001.
nije evidentirano
objavljeno
Podaci o matičnoj publikaciji
26th International Herpesvirus Workshop, Regensburg, Germany
Regensburg:
Podaci o skupu
26th International Herpesvirus Workshop
predavanje
27.07.2001-02.08.2001
Regensburg, Njemačka