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• W2110132503 abstract "Mycobacterium tuberculosis infection elicits antigen-specific CD8(+) T cells that are required to control disease. It is unknown how the major histocompatibility complex class I (MHC-I) pathway samples mycobacterial antigens. CFP10 and ESAT6 are important virulence factors secreted by M. tuberculosis, and they are immunodominant targets of the human and murine T-cell response. Here, we test the hypothesis that CFP10 secretion by M. tuberculosis is required for the priming of CD8(+) T cells in vivo. Our results reveal an explicit dependence upon the bacterial secretion of the CFP10 antigen for the induction of antigen-specific CD8(+) T cells in vivo. By using well-defined M. tuberculosis mutants and carefully controlling for virulence, we show that ESX-1 function is required for the priming of CD8(+) T cells specific for CFP10. CD4(+) and CD8(+) T-cell responses to mycobacterial antigens secreted independently of ESX-1 were unaffected, suggesting that ESX-1-dependent phagosomal escape is not required for CD8(+) T-cell priming during infection. We propose that the overrepresentation of secreted proteins as dominant targets of the CD8(+) T-cell response during M. tuberculosis infection is a consequence of their preferential sampling by the MHC-I pathway. The implications of these findings should be considered in all models of antigen presentation during M. tuberculosis infection and in vaccine development." @default.
• W2110132503 created "2016-06-24" @default.
• W2110132503 creator A5022168346 @default.
• W2110132503 creator A5036239340 @default.
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• W2110132503 date "2008-09-01" @default.
• W2110132503 modified "2023-09-25" @default.
• W2110132503 title "Bacterial Protein Secretion Is Required for Priming of CD8⁺T Cells Specific for the<i>Mycobacterium tuberculosis</i>Antigen CFP10" @default.
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• W2110132503 doi "https://doi.org/10.1128/iai.00307-08" @default.
• W2110132503 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2519428" @default.
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• W2110132503 hasPublicationYear "2008" @default.
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