MAIT cells are activated during human viral infections

van Wilgenburg, B. et al. (2016) MAIT cells are activated during human viral infections. Nature Communications, 7, 11653. (doi: 10.1038/ncomms11653) (PMID:27337592) (PMCID:PMC4931007)

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Abstract

Mucosal-associated invariant T (MAIT) cells are abundant in humans and recognize bacterial ligands. Here, we demonstrate that MAIT cells are also activated during human viral infections in vivo. MAIT cells activation was observed during infection with dengue virus, hepatitis C virus and influenza virus. This activation—driving cytokine release and Granzyme B upregulation—is TCR-independent but dependent on IL-18 in synergy with IL-12, IL-15 and/or interferon-α/β. IL-18 levels and MAIT cell activation correlate with disease severity in acute dengue infection. Furthermore, HCV treatment with interferon-α leads to specific MAIT cell activation in vivo in parallel with an enhanced therapeutic response. Moreover, TCR-independent activation of MAIT cells leads to a reduction of HCV replication in vitro mediated by IFN-γ. Together these data demonstrate MAIT cells are activated following viral infections, and suggest a potential role in both host defence and immunopathology.

Item Type:Articles
Status:Published
Refereed:Yes
Glasgow Author(s) Enlighten ID:Hutchinson, Dr Edward
Authors: van Wilgenburg, B., Scherwitzl, I., Hutchinson, E. C., Leng, T., Kurioka, A., Kulicke, C., de Lara, C., Cole, S., Vasanawathana, S., Limpitikul, W., Malasit, P., Young, D., Denney, L., STOP-HCV consortium, , Moore, M. D., Fabris, P., Giordani, M. T., Oo, Y. H., Laidlaw, S. M., Dustin, L. B., Ho, L.-P., Thompson, F. M., Ramamurthy, N., Mongkolsapaya, J., Willberg, C. B., Screaton, G. R., and Klenerman, P.
College/School:College of Medical Veterinary and Life Sciences > School of Infection & Immunity
College of Medical Veterinary and Life Sciences > School of Infection & Immunity > Centre for Virus Research
Journal Name:Nature Communications
Publisher:Nature Research
ISSN:2041-1723
ISSN (Online):2041-1723
Copyright Holders:Copyright © 2016 The Authors
First Published:First published in Nature Communications 7:11653
Publisher Policy:Reproduced under a Creative Commons License

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