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The mouse cytomegalovirus m152 gene product mediates evasion from immune control through MHC class I restricted T lymphocytes in vivo (CROSBI ID 467349)

Prilog sa skupa u zborniku | sažetak izlaganja sa skupa

Krmpotić, Astrid ; Messerle, Martin ; Crnković, Irena ; Polić, Bojan ; Jonjić, Stipan ; Koszinowski, Ulrich H. 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-x

Podaci o odgovornosti

Krmpotić, Astrid ; Messerle, Martin ; Crnković, Irena ; Polić, Bojan ; Jonjić, Stipan ; Koszinowski, Ulrich H.

engleski

The mouse cytomegalovirus m152 gene product mediates evasion from immune control through MHC class I restricted T lymphocytes in vivo

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.

cytomegalovirus; m152 gene; immunoevasion

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Podaci o prilogu

140-140-x.

1999.

nije evidentirano

objavljeno

Podaci o matičnoj publikaciji

Journal of Clinical Virology, Abstracts of the 7th International Cytomegalovirus Workshop

Drew, Lawrence W ; Leinikki, Pauli

Brighton: Elsevier

Podaci o skupu

7th International Cytomegalovirus Workshop

predavanje

28.04.1999-01.05.1999

Brighton, Ujedinjeno Kraljevstvo

Povezanost rada

Temeljne medicinske znanosti, Kliničke medicinske znanosti