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The MCMV m04 protein plays a key role in prevention of NK cell activation via a "missing self" mechanism (CROSBI ID 548167)

Prilog sa skupa u zborniku | sažetak izlaganja sa skupa | međunarodna recenzija

Babić, Marina ; Pyzik, M ; Krmpotić, Astrid ; Vidal, S.M. ; Jonjić, Stipan The MCMV m04 protein plays a key role in prevention of NK cell activation via a "missing self" mechanism // 12th International CMV/BetaHerpesvirus Workshop May 10-14, 2009 Boston, Massachusettes / Kowalik, T ; Compton, T. (ur.). Boston (MA), 2009. str. 3.01-3.01

Podaci o odgovornosti

Babić, Marina ; Pyzik, M ; Krmpotić, Astrid ; Vidal, S.M. ; Jonjić, Stipan

engleski

The MCMV m04 protein plays a key role in prevention of NK cell activation via a "missing self" mechanism

The ability of herpesviruses to regulate NK cells is perhaps best illustrated in mice infected with mouse cytomegalovirus (MCMV). Like many other viruses, MCMV downregulates MHC class I molecules in order to compromise the CD8 T cell response. Since this function should sensitize the infected cells to NK cells via "missing self"-dependent mechanisms, the virus had to deal with this threat. Unlike two other MCMV regulators of MHC class I molecules (m06, m152), the m04 does not prevent MHC class I expression, but in contrast, it binds to MHC class I, forming complexes that reach the cell surface (Kleijnen et al., EMBO J, 1997.). Based on this, it has been proposed that this function of m04 may serve the virus to inhibit NK cells by providing ligands to inhibitory NK cell receptors. We have now evidence that the virus lacking m04 is attenuated in NK cell- and MHC class I-dependent manner in several mouse strains. Furthermore, by using the reporter cell assay, we have evidence that the presence of m04 can rescue the engagement of inhibitory Ly49 receptor, as compared to the situation when the cells are infected with the virus lacking m04, but possessing two other inhibitors of MHC class I molecules. Interestingly, some mouse strains possess the activating Ly49 receptor specific for MHC class I expressed in complex with m04. We have recently shown that the Ly49P recognition of MCMV-infected cells expressing H2-Dk and m04 is associated with NK cell-mediated resistance in the MA/My mouse

MCMV; m04; NK

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Podaci o prilogu

3.01-3.01.

2009.

objavljeno

Podaci o matičnoj publikaciji

12th International CMV/BetaHerpesvirus Workshop May 10-14, 2009 Boston, Massachusettes

Kowalik, T ; Compton, T.

Boston (MA):

Podaci o skupu

12th International CMV/BetaHerpesvirus Workshop May 10-14, 2009 Boston, Massachusettes

ostalo

10.05.2009-14.05.2009

Boston (MA), Sjedinjene Američke Države

Povezanost rada

Temeljne medicinske znanosti