Journal
JOURNAL OF CLINICAL INVESTIGATION
Volume 117, Issue 8, Pages 2279-2288Publisher
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI31947
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Funding
- NCI NIH HHS [CA 13330, P30 CA013330] Funding Source: Medline
- NIAID NIH HHS [R01 AI054697, AI063537, AI54540, AI054697, HHSN266200400091C, R01 AI054540, P01 AI063537, P30 AI051519, AI 051519] Funding Source: Medline
- PHS HHS [HHSN266200400091C] Funding Source: Medline
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The inhibition of apoptosis of infected host cells is a well-known but poorly understood function of pathogenic mycobacteria. We show that inactivation of the secA2 gene in Mycobacterium tuberculosis, which encodes a component of a virulence-associated protein secretion system, enhanced the apoptosis of infected macrophages by diminishing secretion of mycobacterial superoxide dismutase. Deletion of secA2 markedly increased priming of antigen-specific CD8(+) T cells in vivo, and vaccination of mice and guinea pigs with a secA2 mutant significantly increased resistance to M. tuberculosis challenge compared with standard M. bovis bacille Calmette-Guerin vaccination. Our results define a mechanism for a key immune evasion strategy of M. tuberculosis and provide what we believe to be a novel approach for improving mycobacterial vaccines.
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