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Eur J Immunol. 2016 Feb;46(2):303-6. doi: 10.1002/eji.201546225.

Inflammation and the coagulation system in tuberculosis: Tissue Factor leads the dance.

Author information

1
Central Laboratory for Advanced Diagnosis and Biomedical Research, Università di Palermo, Palermo, Italy.
2
Dipartimento di Biopatologia e Biotecnologie Mediche, Università di Palermo, Palermo, Italy.

Abstract

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.

KEYWORDS:

Macrophages; Mycobacterium tuberculosis; Tissue Factor; Tuberculosis

PMID:
26763085
DOI:
10.1002/eji.201546225
[Indexed for MEDLINE]
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