Rapid interferon independent expression of IFITM3 following T cell activation protects cells from influenza virus infection.

Interferon-induced transmembrane protein 3 (IFITM3) is a potent antiviral protein that enhances cellular resistance to a variety of pathogens, including influenza virus. Classically defined as an interferon-stimulated gene, expression of IFITM3 on cells is rapidly up-regulated in response to type I...

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Main Authors: James G Bedford, Meredith O'Keeffe, Patrick C Reading, Linda M Wakim
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2019-01-01
Series:PLoS ONE
Online Access:https://doi.org/10.1371/journal.pone.0210132
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spelling doaj-eead45276cd146e6910e50dd591f5d652021-03-03T20:57:53ZengPublic Library of Science (PLoS)PLoS ONE1932-62032019-01-01141e021013210.1371/journal.pone.0210132Rapid interferon independent expression of IFITM3 following T cell activation protects cells from influenza virus infection.James G BedfordMeredith O'KeeffePatrick C ReadingLinda M WakimInterferon-induced transmembrane protein 3 (IFITM3) is a potent antiviral protein that enhances cellular resistance to a variety of pathogens, including influenza virus. Classically defined as an interferon-stimulated gene, expression of IFITM3 on cells is rapidly up-regulated in response to type I and II interferon. Here we found that IFITM3 is rapidly up-regulated by T cells following their activation and this occurred independently of type I and II interferon and the interferon regulatory factors 3 and 7. Up-regulation of IFITM3 on effector T cells protected these cells from virus infection and imparted a survival advantage at sites of virus infection. Our results show that IFITM3 expression on effector T cells is crucial for these cells to mediate their effector function and highlights an interferon independent pathway for the induction of IFITM3 which, if targeted, could be an effective approach to harness the activity of IFITM3 for infection prevention.https://doi.org/10.1371/journal.pone.0210132
collection DOAJ
language English
format Article
sources DOAJ
author James G Bedford
Meredith O'Keeffe
Patrick C Reading
Linda M Wakim
spellingShingle James G Bedford
Meredith O'Keeffe
Patrick C Reading
Linda M Wakim
Rapid interferon independent expression of IFITM3 following T cell activation protects cells from influenza virus infection.
PLoS ONE
author_facet James G Bedford
Meredith O'Keeffe
Patrick C Reading
Linda M Wakim
author_sort James G Bedford
title Rapid interferon independent expression of IFITM3 following T cell activation protects cells from influenza virus infection.
title_short Rapid interferon independent expression of IFITM3 following T cell activation protects cells from influenza virus infection.
title_full Rapid interferon independent expression of IFITM3 following T cell activation protects cells from influenza virus infection.
title_fullStr Rapid interferon independent expression of IFITM3 following T cell activation protects cells from influenza virus infection.
title_full_unstemmed Rapid interferon independent expression of IFITM3 following T cell activation protects cells from influenza virus infection.
title_sort rapid interferon independent expression of ifitm3 following t cell activation protects cells from influenza virus infection.
publisher Public Library of Science (PLoS)
series PLoS ONE
issn 1932-6203
publishDate 2019-01-01
description Interferon-induced transmembrane protein 3 (IFITM3) is a potent antiviral protein that enhances cellular resistance to a variety of pathogens, including influenza virus. Classically defined as an interferon-stimulated gene, expression of IFITM3 on cells is rapidly up-regulated in response to type I and II interferon. Here we found that IFITM3 is rapidly up-regulated by T cells following their activation and this occurred independently of type I and II interferon and the interferon regulatory factors 3 and 7. Up-regulation of IFITM3 on effector T cells protected these cells from virus infection and imparted a survival advantage at sites of virus infection. Our results show that IFITM3 expression on effector T cells is crucial for these cells to mediate their effector function and highlights an interferon independent pathway for the induction of IFITM3 which, if targeted, could be an effective approach to harness the activity of IFITM3 for infection prevention.
url https://doi.org/10.1371/journal.pone.0210132
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