Pregled bibliografske jedinice broj: 16979
The mouse cytomegalovirus m152 gene product mediates evasion from immune control through MHC class I restricted T lymphocytes in vivo
The mouse cytomegalovirus m152 gene product mediates evasion from immune control through MHC class I restricted T lymphocytes in vivo // Journal of Clinical Virology, Abstracts of the 7th International Cytomegalovirus Workshop / Drew, Lawrence W ; Leinikki, Pauli (ur.).
Brighton: Elsevier, 1999. str. 140-140 (predavanje, nije recenziran, sažetak, znanstveni)
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Naslov
The mouse cytomegalovirus m152 gene product mediates evasion from immune control through MHC class I restricted T lymphocytes in vivo
Autori
Krmpotić, Astrid ; Messerle, Martin ; Crnković, Irena ; Polić, Bojan ; Jonjić, Stipan ; Koszinowski, Ulrich H.
Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni
Izvornik
Journal of Clinical Virology, Abstracts of the 7th International Cytomegalovirus Workshop
/ Drew, Lawrence W ; Leinikki, Pauli - Brighton : Elsevier, 1999, 140-140
Skup
7th International Cytomegalovirus Workshop
Mjesto i datum
Brighton, Ujedinjeno Kraljevstvo, 28.04.1999. - 01.05.1999
Vrsta sudjelovanja
Predavanje
Vrsta recenzije
Nije recenziran
Ključne riječi
cytomegalovirus; m152 gene; immunoevasion
Sažetak
The murine cytomegalovirus (MCMV) glycoprotein (gp40) encoded by the m152 gene blocks export of MHC class I complexes from the ERGIC/cis-Golgi compartment, and thereby prevents the presentation of viral antigens to cytotoxic T lymphocytes (Ziegler,1997). A recombinant MCMV strain harboring deletion of the m152 gene and the corresponding recombinant revertant virus strain were constructed to investigate the biological significance of this gene product in vivo. Recombinant viruses were produced using cre-loxP recombination system and selected on the basis of lacZ gene expression. Deletion of the m152 gene had no effect on virus growth in primary fibroblast cell culture. As expected for its hypothetical role in immunoevasion m152 deletion mutant strain replicated to lower titers and exhibited an attenuated disease course in vivo. By advent of highly sensitive model of B cell deficient mice and selective in vivo depletion of T lymphocyte subsets we could demonstrate that m152 deletion mutant strain is more susceptible to control by CD8+ T lymphocytes as compared to its revertant virus strain. In contrast, both viruses replicated to equal titers in CD8-subset-deficient mice as well as in mice deficient of MHC class I molecules. The resolution of primary MCMV infection of immunocompromised host by adoptively transferred nonprimed T lymphocytes is accelarated in recipients infected with m152 deletion mutant virus suggesting that the lack of respective immunoevasion function sensitize the virus to primary response by nażve T lymphocytes. Altogether, the results demonstrated that expression of a single viral glycoprotein involved in process of antigen presentation in context of MHC class I molecules strongly modulates the function of CD8+ T lymphocytes in vivo.
Izvorni jezik
Engleski
Znanstvena područja
Temeljne medicinske znanosti, Kliničke medicinske znanosti