Pregled bibliografske jedinice broj: 482850
Cytomegalovirus immunoevasin reveals the physiological role of “missing self” recognition in natural killer cell dependent virus control in vivo
Cytomegalovirus immunoevasin reveals the physiological role of “missing self” recognition in natural killer cell dependent virus control in vivo // 35th Annual International Herpesvirus Workshop (IHW 2010) / Hutt-Fletcher, Lindsey ; Yurochko, Andrew (ur.).
Salt Lake City (UT): University of Utah, 2010. (plenarno, međunarodna recenzija, pp prezentacija, znanstveni)
CROSBI ID: 482850 Za ispravke kontaktirajte CROSBI podršku putem web obrasca
Naslov
Cytomegalovirus immunoevasin reveals the physiological role of “missing self” recognition in natural killer cell dependent virus control in vivo
Autori
Jonjić, Stipan
Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, pp prezentacija, znanstveni
Izvornik
35th Annual International Herpesvirus Workshop (IHW 2010)
/ Hutt-Fletcher, Lindsey ; Yurochko, Andrew - Salt Lake City (UT) : University of Utah, 2010
Skup
Annual International Herpesvirus Workshop (35 ; 2010)
Mjesto i datum
Salt Lake City (UT), Sjedinjene Američke Države, 24.07.2010. - 29.07.2010
Vrsta sudjelovanja
Plenarno
Vrsta recenzije
Međunarodna recenzija
Ključne riječi
cytomegalovirus; missing self; NK cell
Sažetak
Cytomegaloviruses (CMVs) are renowned for interfering with the immune system of their hosts. To sidestep antigen presentation and destruction by CD8+ T cells, these viruses reduce expression of major histocompatibility complex class I (MHC I) molecules. However, this process sensitizes the virus-infected cells to natural killer (NK) cell–mediated killing via the “missing self” axis. Mouse cytomegalovirus (MCMV) uses m152 and m06 encoded proteins to inhibit surface expression of MHC I molecules. In addition, it encodes another protein, m04, which forms complexes with MHC I and escorts them to the cell surface. This mechanism is believed to prevent NK cell activation and killing by restoring the “self” signature and allowing the engagement of inhibitory Ly49 receptors on NK cells. Here we show that MCMV lacking m04 was attenuated in an NK cell– and MHC I–dependent manner. NK cell–mediated control of the infection was dependent on the presence of NK cell subsets expressing different inhibitory Ly49 receptors. In addition to providing evidence for immunoevasion strategies used by CMVs to avoid NK cell control via the missing-self pathway, our study is the first to demonstrate that missing self–dependent NK cell activation is biologically relevant in the protection against viral infection in vivo.
Izvorni jezik
Engleski
Znanstvena područja
Temeljne medicinske znanosti
POVEZANOST RADA
Projekti:
062-0621261-1263 - Molekularni mehanizmi citomegalovirusnog izmicanja imunološkom nadzoru (Jonjić, Stipan, MZOS ) ( CroRIS)
Ustanove:
Medicinski fakultet, Rijeka
Profili:
Stipan Jonjić
(autor)