固有免疫细胞对结核分枝杆菌的免疫识别

doi:10.3969/j.issn.1000-6621.2015.02.014

摘要/Abstract

摘要： 由结核分枝杆菌感染引起的肺结核已成为非常重要的健康问题，全球每年因结核病死亡的患者超过200万例。机体的固有免疫在抵抗结核分枝杆菌感染过程中发挥了重要作用。多种模式识别受体参与了固有免疫细胞对结核分枝杆菌的识别，包括Toll样受体（TLR）、C-型凝集素受体及核苷酸结合寡聚化结构域（NOD）样受体。在Toll样受体中，TLR2、TLR4及TLR9及其接头分子髓样分化因子（MyD88）在启动针对结核分枝杆菌感染的免疫应答方面发挥了主要作用。另外，其他的模式识别受体，如NOD2、树突状细胞相关性C型植物血凝素-1（Dectin-1）、甘露糖受体及树突状细胞表面特异性C型凝集素-细胞间黏附分子3结合非整合素分子（DC-SIGN）也参与对结核分枝杆菌的识别。流行病学研究发现，模式识别受体基因突变影响机体对结核分枝杆菌感染的易感性。因此，深入研究模式识别受体对结核分枝杆菌的识别特点及基因多态性分布特征，对加深了解结核分枝杆菌致病特点、设计新型抗结核的免疫制剂可提供理论支持。

关键词: 受体, 模式识别, 结核分枝杆菌, 免疫, 细胞

Abstract: Tuberculosis (TB), caused by Mycobacterium tuberculosis (Mtb), is a major health problem, with over 2 million deaths each year in the world. Innate immunity plays an important role in the host defense against Mtb. Several classes of pattern recognition receptors (PPRs) expressed on innate immune cells are involved in the recognition of Mtb, including Toll-like receptors (TLRs), C-type lectin receptors (CLRs), and NOD-like receptors (NLRs). Among the TLR family, TLR2, TLR4, and TLR9 and their adaptor molecule MyD88 play a leading role in the initiation of the immune response against tuberculosis. In addition to TLRs, other PRRs such as NOD2, Dectin-1, Mannose receptor, and DC-SIGN are also involved in the recognition of Mtb. Human epidemiological studies reveal that genetic variation in genes encoding for PRRs in uences disease susceptibility. Therefore, to explore in depth on the recognition characteristics of PRRs and the distribution of gene polymorphism, does not only lead to a better understanding of the pathogenesis of tuberculosis but also may contribute to the design of novel immunotherapeutic strategies.

Key words: Receptors, pattern recognition, Mycobacterium tuberculosis, Immunity, cellular

吴小娥，陈晶，宋淑霞. 固有免疫细胞对结核分枝杆菌的免疫识别[J]. 中国防痨杂志, 2015, 37(2): 189-193. doi: 10.3969/j.issn.1000-6621.2015.02.014

WU Xiao-e，CHEN Jing，SONG Shu-xia. Innate immune recognition of Mycobacterium tuberculosis[J]. Chinese Journal of Antituberculosis, 2015, 37(2): 189-193. doi: 10.3969/j.issn.1000-6621.2015.02.014

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