Monin Leticia, Khader Shabaana A
Department of Molecular Microbiology, Washington University School of Medicine, 660 South Euclid Avenue, St. Louis, MO 63110, USA; Richard King Mellon Foundation Institute for Pediatric Research, Children's Hospital of Pittsburgh of UPMC, 4401 Penn Avenue, Pittsburgh, PA 15224, USA.
Department of Molecular Microbiology, Washington University School of Medicine, 660 South Euclid Avenue, St. Louis, MO 63110, USA.
Semin Immunol. 2014 Dec;26(6):552-8. doi: 10.1016/j.smim.2014.09.004. Epub 2014 Oct 22.
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).
结核分枝杆菌（Mtb）感染了全球约三分之一的人口，大多数感染者表现为潜伏无症状感染，而5-10%的感染者会发展为活动性肺结核。过去二十年的研究阐明了介导Mtb控制的关键宿主免疫机制。其中，趋化因子与导致Mtb遏制的众多关键过程相关，从髓样细胞募集到肺部到适应性免疫激活、保护性肉芽肿形成和疫苗召回反应。然而，几种关键趋化因子介质的失衡会改变促进分枝杆菌遏制的细胞因子和细胞反应的微妙平衡，反而会导致终末期组织破坏和Mtb感染扩散。在本综述中，我们将描述趋化因子在宿主对Mtb感染和Mtb遏制反应中的最新见解（好的方面）、趋化因子在结核病期间促成炎症的作用（坏的方面）以及趋化因子在导致空洞形成和肺部病理中的作用（丑陋的方面）。
