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.
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