期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 97, 期 15, 页码 8455-8460出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.150240097
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资金
- NCI NIH HHS [P30 CA021765, CA 21765] Funding Source: Medline
- NIAID NIH HHS [R01 AI042373, AI38359, AI42373] Funding Source: Medline
The gamma-herpesviruses, in contrast to the alpha- and beta-herpesviruses. are not known to inhibit antigen presentation to CD8(+) cytotoxic T lymphocytes (CTLs) during lytic cycle replication. However, murine gamma-herpesvirus 68 causes a chronic lytic infection in CD4(+) T cell-deficient mice despite the persistence of a substantial CTL response, suggesting that CTL evasion occurs. Here we show that, distinct from host protein synthesis shutoff, gamma-herpesvirus 68 down-regulates surface MHC class I expression on lytically infected fibroblasts and inhibits their recognition by antigen-specific CTLs, The viral K3 gene, encoding a zinc-finger-containing protein. dramatically reduced the half-life of nascent class I molecules and the level of surface MHC class I expression and was by itself sufficient to block antigen presentation. The homologous K3 and Ks genes of the related Kaposi's sarcoma-associated virus also inhibited antigen presentation and decreased cell surface expression of HLA class I antigens. Thus it appears that an immune evasion strategy shared by at least two gamma-herpesviruses allows continued lytic infection in the face of strong CTL immunity.
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