Brucella abortus induces intracellular retention of MHC-I molecules in human macrophages down-modulating cytotoxic CD8(+) T cell responses.
作者： Paula Barrionuevo , M. Victoria Delpino , Roberto G. Pozner , Lis N. Velásquez , Juliana Cassataro
DOI: 10.1111/CMI.12058
关键词: Cytotoxic T cell 、 Immune system 、 CD8 、 Microbiology 、 Major histocompatibility complex 、 Molecular biology 、 Interferon gamma 、 Biology 、 Antigen-presenting cell 、 Interleukin 21 、 MHC class I
摘要: Brucella abortus elicits a vigorous Th1 immune response which activates cytotoxic T lymphocytes. However, B. persists in its hosts the presence of CD8(+) cells, establishing chronic infection. Here, we report that infection human monocytes/macrophages inhibited IFN-γ-induced MHC-I cell surface expression. This phenomenon was dependent on metabolically active viable bacteria. down-modulation correlated with development diminished as evidenced by reduced expression activation marker CD107a lymphocytes and percentage IFN-γ-producing cells. Inhibition not due to changes protein synthesis. Rather, observed upon molecules were retained within Golgi apparatus. Overall, these results describe novel mechanism based intracellular sequestration whereby would avoid responses, evading their immunological surveillance.
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