Enhanced Priming of Adaptive Immunity by a Proapoptotic Mutant of Mycobacterium Tuberculosis.
From: Department of Microbiology and Immunology and Howard Hughes Medical Institute, Albert Einstein College of Medicine, New York, New York 10461, USA.
The Journal of clinical investigation
- Publish Date: Aug 2007
- ISSN: 0021-9738
- Volume: 117
- Issue: 8
- Pages: 2279-88
- Medium: Print
- Language: English
- Citation (JAMA): Hinchey Joseph, Lee Sunhee, Jeon Bo Y, et al. Enhanced Priming of Adaptive Immunity by a Proapoptotic Mutant of Mycobacterium Tuberculosis.. J. Clin. Invest. Aug 2007;117:2279-88
Abstract
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-Guérin 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.
Mesh Headings (Keywords): Adenosine Triphosphatases, Animals, Bacterial Proteins, Cell Line, Gene Deletion, Guinea Pigs, Humans, Macrophages, Membrane Transport Proteins, Mice, Mice, Inbred BALB C, Mycobacterium bovis, Mycobacterium tuberculosis, Superoxide Dismutase, Tuberculosis, Tuberculosis Vaccines
Check for Full Text / PubMed Unique Identifier (PMID): 17671656
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