Pregled bibliografske jedinice broj: 385072
Ly49P recognition of cytomegalovirus-infected cells expressing H2-Dk and CMV-encoded m04 correlates with the NK cell antiviral response
Ly49P recognition of cytomegalovirus-infected cells expressing H2-Dk and CMV-encoded m04 correlates with the NK cell antiviral response // Journal of Experimental Medicine, 206 (2009), 3; 515-523 doi:10.1084/jem.20080954 (međunarodna recenzija, članak, znanstveni)
CROSBI ID: 385072 Za ispravke kontaktirajte CROSBI podršku putem web obrasca
Naslov
Ly49P recognition of cytomegalovirus-infected cells expressing H2-Dk and CMV-encoded m04 correlates with the NK cell antiviral response
Autori
Kielczewska, A. ; Pyzik, M. ; Sun, T. ; Krmpotić, Astrid ; Lodoen, M. B. ; Munks, M. W. ; Babić, Marina ; Hill, A. B. ; Koszinowski, U. H. ; Jonjić, Stipan ; Lanier, L. ; Vidal, S. M.
Izvornik
Journal of Experimental Medicine (0022-1007) 206
(2009), 3;
515-523
Vrsta, podvrsta i kategorija rada
Radovi u časopisima, članak, znanstveni
Ključne riječi
antiviral response; CMV; NK cells
Sažetak
Natural killer (NK) cells are crucial in resistance to certain viral infections, but the mechanisms used to recognize infected cells remain largely unknown. Here, we show that the activating Ly49P receptor recognizes cells infected with mouse cytomegalovirus (MCMV) by a process that requires the presence of H2-D(k) and the MCMV m04 protein. Using H2 chimeras between H2-D(b) and -D(k), we demonstrate that the H2-D(k) peptide-binding platform is required for Ly49P recognition. We identified m04 as a viral component necessary for recognition using a panel of MCMV-deletion mutant viruses and complementation of m04-deletion mutant (Deltam04) virus infection. MA/My mice, which express Ly49P and H2-D(k), are resistant to MCMV ; however, infection with Deltam04 MCMV abrogates resistance. Depletion of NK cells in MA/My mice abrogates their resistance to wild-type MCMV infection, but does not significantly affect viral titers in mice infected with Deltam04 virus, implicating NK cells in host protection through m04-dependent recognition. These findings reveal a novel mechanism of major histocompatability complex class I-restricted recognition of virally infected cells by an activating NK cell receptor.
Izvorni jezik
Engleski
Znanstvena područja
Temeljne medicinske znanosti
POVEZANOST RADA
Projekti:
062-0621261-1263 - Molekularni mehanizmi citomegalovirusnog izmicanja imunološkom nadzoru (Jonjić, Stipan, MZOS ) ( CroRIS)
062-0621261-1268 - Uloga imunosubverzivnih citomegalovirusnih gena u latenciji (Krmpotić, Astrid, MZOS ) ( CroRIS)
Ustanove:
Medicinski fakultet, Rijeka
Citiraj ovu publikaciju:
Časopis indeksira:
- Current Contents Connect (CCC)
- Web of Science Core Collection (WoSCC)
- Science Citation Index Expanded (SCI-EXP)
- SCI-EXP, SSCI i/ili A&HCI
- Scopus
- MEDLINE