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本文引用的文献

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CD43 controls the intracellular growth of Mycobacterium tuberculosis through the induction of TNF-alpha-mediated apoptosis.CD43通过诱导肿瘤坏死因子-α介导的细胞凋亡来控制结核分枝杆菌的细胞内生长。
Cell Microbiol. 2008 Oct;10(10):2105-17. doi: 10.1111/j.1462-5822.2008.01194.x. Epub 2008 Jul 10.
2
Hypercholesterolemia impairs immunity to tuberculosis.高胆固醇血症会损害对结核病的免疫力。
Infect Immun. 2008 Aug;76(8):3464-72. doi: 10.1128/IAI.00037-08. Epub 2008 May 27.
3
Mycobacterial interaction with innate receptors: TLRs, C-type lectins, and NLRs.分枝杆菌与天然免疫受体的相互作用:Toll样受体、C型凝集素和NOD样受体。
Curr Opin Infect Dis. 2008 Jun;21(3):279-86. doi: 10.1097/QCO.0b013e3282f88b5d.
4
CD14 contributes to pulmonary inflammation and mortality during murine tuberculosis.CD14在小鼠结核病期间会导致肺部炎症和死亡。
Immunology. 2008 Oct;125(2):272-9. doi: 10.1111/j.1365-2567.2008.02840.x. Epub 2008 Apr 3.
5
Mycobacterium abscessus activates the macrophage innate immune response via a physical and functional interaction between TLR2 and dectin-1.脓肿分枝杆菌通过Toll样受体2(TLR2)与树突状细胞特异性细胞内黏附分子-3结合非整合素(dectin-1)之间的物理和功能相互作用激活巨噬细胞固有免疫反应。
Cell Microbiol. 2008 Aug;10(8):1608-21. doi: 10.1111/j.1462-5822.2008.01151.x. Epub 2008 Mar 26.
6
Role of C-type lectins in mycobacterial infections.C型凝集素在分枝杆菌感染中的作用。
Curr Drug Targets. 2008 Feb;9(2):102-12. doi: 10.2174/138945008783502467.
7
Containment of aerogenic Mycobacterium tuberculosis infection in mice does not require MyD88 adaptor function for TLR2, -4 and -9.在小鼠中,对空气传播的结核分枝杆菌感染的控制并不需要Toll样受体2、4和9的MyD88衔接蛋白功能。
Eur J Immunol. 2008 Mar;38(3):680-94. doi: 10.1002/eji.200736458.
8
Syk kinase is required for collaborative cytokine production induced through Dectin-1 and Toll-like receptors.Syk激酶是通过Dectin-1和Toll样受体诱导协同细胞因子产生所必需的。
Eur J Immunol. 2008 Feb;38(2):500-6. doi: 10.1002/eji.200737741.
9
CD209 genetic polymorphism and tuberculosis disease.CD209基因多态性与结核病
PLoS One. 2008 Jan 2;3(1):e1388. doi: 10.1371/journal.pone.0001388.
10
CD14 C(-159)T polymorphism is a risk factor for development of pulmonary tuberculosis.CD14基因C(-159)T多态性是肺结核发病的一个危险因素。
J Infect Dis. 2007 Dec 1;196(11):1698-706. doi: 10.1086/522147. Epub 2007 Oct 25.

吞噬细胞对结核分枝杆菌的非调理作用识别。

Non-opsonic recognition of Mycobacterium tuberculosis by phagocytes.

机构信息

Institute for Infectious Diseases and Molecular Medicine, Division of Immunology, CLS, Faculty of Health Sciences, University of Cape Town, South Africa.

出版信息

J Innate Immun. 2009;1(3):231-43. doi: 10.1159/000173703. Epub 2008 Nov 12.

DOI:10.1159/000173703
PMID:20375581
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7312845/
Abstract

The interactions between Mycobacterium tuberculosis and host phagocytes such as macrophages and dendritic cells are central to both immunity and pathogenesis. Many receptors have been implicated in recognition and binding of M. tuberculosis such as the mannose receptor, dendritic-cell-specific intercellular adhesion molecule-3 grabbing nonintegrin, dectin-1 and complement receptor 3 as well as Toll-like receptors, scavenger receptors and CD14. While in vitro studies have demonstrated clear roles for particular receptor(s), in vivo work in receptor-deficient animals often revealed only a minor, or no role, in infection with M. tuberculosis. The initial encounter of phagocytic cells with myco- bacteria appears to be complex and depends on various parameters. It seems likely that infection with M. tuberculosis does not occur via a single receptor-mediated pathway. Rather, multiple receptors play different roles in M. tuberculosis infection, and the overall effect depends on the expression and availability of a particular receptor on a particular cell type and its triggered downstream responses. Moreover, the role of membrane cholesterol for M. tuberculosis interactions with phagocytes adds to the complexity of mycobacterial recognition and response. This review summarizes current knowledge on non-opsonic receptors involved in binding of mycobacteria and discusses the contribution of individual receptors to the recognition process.

摘要

分枝杆菌与宿主吞噬细胞(如巨噬细胞和树突状细胞)之间的相互作用是免疫和发病机制的核心。许多受体已被牵涉到分枝杆菌的识别和结合中,如甘露糖受体、树突状细胞特异性细胞间黏附分子-3 抓取非整合素、dectin-1 和补体受体 3 以及 Toll 样受体、清道夫受体和 CD14。虽然体外研究已经证明了特定受体的明确作用,但在受体缺陷动物的体内研究中,分枝杆菌感染的作用往往只有很小,或者没有作用。吞噬细胞与分枝杆菌的初始接触似乎很复杂,取决于各种参数。似乎感染分枝杆菌不是通过单一的受体介导途径发生的。相反,多种受体在分枝杆菌感染中发挥不同的作用,整体效果取决于特定细胞类型上特定受体的表达和可用性及其触发的下游反应。此外,膜胆固醇在分枝杆菌与吞噬细胞相互作用中的作用增加了分枝杆菌识别和反应的复杂性。这篇综述总结了参与分枝杆菌结合的非调理受体的最新知识,并讨论了单个受体对识别过程的贡献。