期刊
CELLULAR MICROBIOLOGY
卷 15, 期 4, 页码 487-502出版社
WILEY-BLACKWELL
DOI: 10.1111/cmi.12058
关键词
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资金
- Agencia Nacional de Promocion Cientifica y Tecnologica (ANPCYT-Argentina) [PICT 2010-0023, 2006-1335, 2006-2180]
- CONICET (Argentina) [PIP 5213, 1390]
- UBA (Argentina) [UBACyT 20020090100083]
Brucella abortus elicits a vigorous Th1 immune response which activates cytotoxic T lymphocytes. However, B.abortus persists in its hosts in the presence of CD8+ T cells, establishing a chronic infection. Here, we report that B.abortus infection of human monocytes/macrophages inhibited the IFN--induced MHC-I cell surface expression. This phenomenon was dependent on metabolically active viable bacteria. MHC-I down-modulation correlated with the development of diminished CD8+ cytotoxic T cell response as evidenced by the reduced expression of the activation marker CD107a on CD8+ T lymphocytes and a diminished percentage of IFN--producing CD8+ T cells. Inhibition of MHC-I expression was not due to changes in protein synthesis. Rather, we observed that upon B.abortus infection MHC-I molecules were retained within the Golgi apparatus. Overall, these results describe a novel mechanism based on the intracellular sequestration of MHC-I molecules whereby B.abortus would avoid CD8+ cytotoxic T cell responses, evading their immunological surveillance.
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