Deng Wanyan, Xie Jianping
Institute of Modern Biopharmaceuticals, State Key Laboratory Breeding Base of Eco-Environment and Bio-Resource of the Three Gorges Area, School of Life Sciences, Southwest University, Beibei, Chongqing, China.
Cell Physiol Biochem. 2012;30(4):953-63. doi: 10.1159/000341472. Epub 2012 Sep 13.
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.
分枝杆菌病原体获得额外特性以扩大其致病性和生存空间。致病性分枝杆菌成分与宿主固有免疫系统受体之间的相互作用对感染结果至关重要，尤其是对巨噬细胞的激活。NOD2（核苷酸结合寡聚化结构域2）是一种细胞内病原体识别传感器，可减弱两种关键的假定宿主细菌杀伤机制：干扰肿瘤坏死因子-α的产生和诱导抗凋亡能力。多项证据表明，NOD2作为分枝杆菌的一种非冗余识别系统，该成功病原体具有多种逃避宿主免疫并导致隐匿性疾病的机制。了解由NOD2信号介导的宿主与病原体之间的复杂相互作用，可能为致病性分枝杆菌的发病机制提供新的见解，并为开发更有效的疫苗和治疗方法提供依据。
