期刊
CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
卷 30, 期 4, 页码 953-963出版社
KARGER
DOI: 10.1159/000341472
关键词
Mycobacterium tuberculosis; NOD2; Sentinel; Innate immune; Tuberculosis
资金
- National natural science foundation [81071316]
- Fundamental Research Funds for the Central Universities [XDJK2009A003]
- New Century Talents in Universities [NCET-11-0703]
- National megaproject for key infectious disease [2008ZX10003-006, 2012ZX10003-003]
- Southwest University [kb2009010, ky2011003]
The Mycobacterium pathogens acquire additional properties to expand their pathogenicity and existence spaces. The interaction between pathogenic Mycobacterium components and receptors of host innate immune system is critical for the infection outcome, particularly for the macrophage activation. NOD2 (Nucleotide binding oligomerization domain 2), an intracellular pathogen recognition sensor, attenuates two key putative host bacterial killing mechanisms: interfering the production of TNF-alpha and inducing resistance to apoptosis. Multiple evidences have shown that NOD2 acts as a non-redundant recognition system of Mycobacterium, a successful pathogen with many mechanisms to evade host immunity and leading to insidious disease. Understanding the complex interaction between host and pathogen mediated by NOD2 signaling, might provide novel insight into the pathogenesis of pathogenic Mycobacterium and inform the development of more effective vaccines and therapeutics. (C) Copyright c 2012 S. Karger AG, Basel
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