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Early production of IL-17A by γδ T cells in the trachea promotes viral clearance during influenza infection in mice

tetano

Editor, Senior Moderator
Eur J Immunol. 2019 Nov 27. doi: 10.1002/eji.201948157. [Epub ahead of print] [h=1]Early production of IL-17A by γδ T cells in the trachea promotes viral clearance during influenza infection in mice.[/h]
Palomino-Segura M[SUP]1,[/SUP][SUP]2[/SUP], Latino I[SUP]1[/SUP], Farsakoglu Y[SUP]3[/SUP], Gonzalez SF[SUP]1[/SUP].
[h=3]Author information[/h] 1 Institute for Research in Biomedicine, Universit? della Svizzera italiana, via Vincenzo Vela 6, CH-6500, Bellinzona, Switzerland. 2 Graduate School of Cellular and Molecular Sciences, Faculty of Medicine, University of Bern, 3012, Bern, Switzerland. 3 Salk Institute for Biological Studies, La Jolla, CA 92037, USA.

[h=3]Abstract[/h] The innate immune response generated against influenza infection is critical for the inhibition of viral dissemination. The trachea contains different types of innate immune cells that protect the respiratory tract from pathogen invasion. Amongst them, γδ T cells have the ability to rapidly generate large amounts of pro-inflammatory cytokines to preserve mucosal barrier homeostasis during infection. However, little is known about their role during the early phase of influenza infection in the airways. In this study we found that, early after infection, γδ T cells are recruited and activated in the trachea and outnumber αβ T cells during the course of the influenza infection that follows. We also showed that the majority of the recruited γδ T cells express the Vγ4 TCR chain and infiltrate in a process that involves the chemokine receptor CXCR3. In addition, we demonstrated that γδ T cells promote the recruitment of protective neutrophils and NK cells to the tracheal mucosa. Altogether, our results highlight the importance of the immune responses mediated by γδ T cells. This article is protected by copyright. All rights reserved.
This article is protected by copyright. All rights reserved.


[h=4]KEYWORDS:[/h] IL-17A; influenza virus; neutrophils; trachea; γδ T cell

PMID: 31777067 DOI: 10.1002/eji.201948157
 
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