Caccamo Nadia, Dieli Francesco
Central Laboratory for Advanced Diagnosis and Biomedical Research, Università di Palermo, Palermo, Italy.
Dipartimento di Biopatologia e Biotecnologie Mediche, Università di Palermo, Palermo, Italy.
Eur J Immunol. 2016 Feb;46(2):303-6. doi: 10.1002/eji.201546225.
Mycobacterium tuberculosis, the causative agent of tuberculosis, drives the formation of granulomas, structures in which both immune cells and the bacterial pathogen cohabit. The most abundant cells in granulomas are macrophages, which contribute as both cells with bactericidal activity and as targets for M. tuberculosis infection and proliferation during the entire course of infection. The mechanisms and factors involved in the regulation and control of macrophage microenvironment-specific polarization and plasticity are not well understood, as some granulomas are able to control bacteria growth and others fail to do so, permitting bacterial spread. In this issue of the European Journal of Immunology, Venkatasubramanian et al. [Eur. J. Immunol. 2016. 46: 464-479] show that mice lacking the tissue factor gene in myeloid cells have augmented M. tuberculosis growth and increased inflammation in the lungs. This suggests that tissue factor, an initiator of coagulation, is important for the generation of fibrin, which supports granuloma formation. This article demonstrates for the first time the involvement of tissue factor in inducing effective immunity against M. tuberculosis, and sheds new lights on the complex interplay between host inflammatory response, the coagulation system, and the control of M. tuberculosis infection.
结核分枝杆菌是结核病的病原体，可促使肉芽肿的形成，在这种结构中免疫细胞和细菌病原体共存。肉芽肿中最丰富的细胞是巨噬细胞，在感染的整个过程中，巨噬细胞既是具有杀菌活性的细胞，又是结核分枝杆菌感染和增殖的靶标。由于一些肉芽肿能够控制细菌生长而另一些则不能，从而导致细菌传播，因此巨噬细胞微环境特异性极化和可塑性的调控机制及相关因素尚未完全明确。在本期《欧洲免疫学杂志》中，Venkatasubramanian等人[《欧洲免疫学杂志》2016年。46: 464 - 479]表明，髓系细胞中缺乏组织因子基因的小鼠，其结核分枝杆菌生长加剧，肺部炎症增加。这表明组织因子作为凝血的启动因子，对纤维蛋白的生成很重要，而纤维蛋白有助于肉芽肿的形成。本文首次证明了组织因子参与诱导针对结核分枝杆菌的有效免疫，并为宿主炎症反应、凝血系统和结核分枝杆菌感染控制之间的复杂相互作用提供了新的线索。
