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Type I interferons in tuberculosis: Foe and occasionally friend. | LitMetric

Type I interferons in tuberculosis: Foe and occasionally friend.

J Exp Med

Laboratory of Immunoregulation and Infection, The Francis Crick Institute, London, England, UK

Published: May 2018

AI Article Synopsis

  • - Tuberculosis is a major global health issue, leading to high mortality rates, and research is still uncovering how infections cause harm or activate protection in the immune system.
  • - Type I interferons (IFN) play complex roles in immunity, with studies indicating they can sometimes worsen tuberculosis by promoting bacterial growth and disease progression.
  • - Recent findings highlight that the effects of type I IFN in tuberculosis depend on specific contexts, suggesting it can have both harmful and protective contributions during the infection process.

Article Abstract

Tuberculosis remains one of the leading causes of mortality worldwide, and, despite its clinical significance, there are still significant gaps in our understanding of pathogenic and protective mechanisms triggered by infection. Type I interferons (IFN) regulate a broad family of genes that either stimulate or inhibit immune function, having both host-protective and detrimental effects, and exhibit well-characterized antiviral activity. Transcriptional studies have uncovered a potential deleterious role for type I IFN in active tuberculosis. Since then, additional studies in human tuberculosis and experimental mouse models of infection support the concept that type I IFN promotes both bacterial expansion and disease pathogenesis. More recently, studies in a different setting have suggested a putative protective role for type I IFN. In this study, we discuss the mechanistic and contextual factors that determine the detrimental versus beneficial outcomes of type I IFN induction during infection, from human disease to experimental mouse models of tuberculosis.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5940272PMC
http://dx.doi.org/10.1084/jem.20180325DOI Listing

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