Chemokines in tuberculosis: the good, the bad and the ugly.

Chemokines in tuberculosis: the good, the bad and the ugly.
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DOI:
10.1016/j.smim.2014.09.004
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发表时间:
2014-12
影响因子:
7.8
通讯作者:
Khader SA
Khader SA
中科院分区:
医学2区
文献类型:
--
作者:
Monin L;Khader SA

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结核分枝杆菌(Mycobacterium tuberculosis,Mtb)感染世界上约三分之一的人口,其中大多数感染个体表现出潜伏的无症状感染,而5-10%的感染个体进展为活动性肺病。过去二十年的研究已经阐明了介导Mtb控制的关键宿主免疫机制。其中,趋化因子与导致Mtb遏制的许多关键过程相关,从骨髓细胞招募到肺中到适应性免疫的激活,保护性肉芽肿的形成和疫苗召回反应。然而,在几个关键的趋化因子介质的不平衡,可以改变细胞因子和细胞反应,促进分枝杆菌遏制微妙的平衡,而不是沉淀终端组织破坏和结核分枝杆菌感染的传播。在这篇综述中,我们将描述最近的见解,在宿主对结核分枝杆菌感染和结核分枝杆菌遏制反应的趋化因子(好),趋化因子在结核病(坏),和趋化因子在驱动空化和肺病理(丑陋)的作用。
Mycobacterium tuberculosis (Mtb) infects about one third of the world’s population, with a majority of infected individuals exhibiting latent asymptomatic infection, while 5–10% of infected individuals progress to active pulmonary disease. Research in the past two decades has elucidated critical host immune mechanisms that mediate Mtb control. Among these, chemokines have been associated with numerous key processes that lead to Mtb containment, from recruitment of myeloid cells into the lung to activation of adaptive immunity, formation of protective granulomas and vaccine recall responses. However, imbalances in several key chemokine mediators can alter the delicate balance of cytokines and cellular responses that promote mycobacterial containment, instead precipitating terminal tissue destruction and spread of Mtb infection. In this review, we will describe recent insights in the involvement of chemokines in host responses to Mtb infection and Mtb containment (the good), chemokines contributing to inflammation during TB (the bad), and the role of chemokines in driving cavitation and lung pathology (the ugly).
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