Abstract
MHC class I-restricted CD8(+) T cells are necessary to mount an immune response against Mycobacterium tuberculosis. M. tuberculosis antigens can enter MHC class I cross-processing pathways through a number of different mechanisms, including via the uptake of antigen-containing apoptotic vesicles released by infected cells. A study in this issue of the JCI by Hinchey and colleagues shows that M. tuberculosis inhibits host cell apoptosis and thus may interfere with optimal cross-priming and action of CD8(+) T cells (see the related article beginning on page 2279). M. tuberculosis genetically modified to induce apoptosis is shown to be more effective in priming CD8(+) T cells in vivo and therefore may be a more effective vaccine against tuberculosis than the currently utilized M. bovis BCG vaccine.
Publication types
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Comment
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Research Support, N.I.H., Extramural
MeSH terms
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Adenosine Triphosphatases* / deficiency
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Animals
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Bacterial Proteins*
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Cell Line
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Gene Deletion*
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Guinea Pigs
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Humans
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Macrophages / immunology*
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Macrophages / microbiology
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Membrane Transport Proteins* / deficiency
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Mice
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Mice, Inbred BALB C
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Mycobacterium bovis / immunology
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Mycobacterium tuberculosis / genetics
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Mycobacterium tuberculosis / immunology*
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Mycobacterium tuberculosis / pathogenicity
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Superoxide Dismutase / genetics
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Superoxide Dismutase / immunology
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Tuberculosis / genetics
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Tuberculosis / immunology*
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Tuberculosis / prevention & control
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Tuberculosis Vaccines / genetics
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Tuberculosis Vaccines / immunology*
Substances
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Bacterial Proteins
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Membrane Transport Proteins
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Tuberculosis Vaccines
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Superoxide Dismutase
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Adenosine Triphosphatases
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SecA2 protein, Mycobacterium