Contribution of NKT cells to the immune response and pathogenesis triggered by respiratory viruses

Human respiratory syncytial virus (hRSV) and human metapneumovirus (hMPV) cause acute respiratory tract infections in children worldwide. Natural killer T (NKT) cells are unconventional T lymphocytes, and their TCRs recognize glycolipids bound to the MHC-I-like molecule, CD1d. These cells modulate t...

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Autores principales: Emma Rey-Jurado, Karen Bohmwald, Nicolás M.S. Gálvez, Daniela Becerra, Steven A. Porcelli, Leandro J. Carreño, Alexis M. Kalergis
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Publicado: Taylor & Francis Group 2020
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spelling oai:doaj.org-article:59c574c9a2d5419cafa11db90d74d5622021-11-17T14:21:58ZContribution of NKT cells to the immune response and pathogenesis triggered by respiratory viruses2150-55942150-560810.1080/21505594.2020.1770492https://doaj.org/article/59c574c9a2d5419cafa11db90d74d5622020-12-01T00:00:00Zhttp://dx.doi.org/10.1080/21505594.2020.1770492https://doaj.org/toc/2150-5594https://doaj.org/toc/2150-5608Human respiratory syncytial virus (hRSV) and human metapneumovirus (hMPV) cause acute respiratory tract infections in children worldwide. Natural killer T (NKT) cells are unconventional T lymphocytes, and their TCRs recognize glycolipids bound to the MHC-I-like molecule, CD1d. These cells modulate the inflammatory response in viral infections. Here, we evaluated the contribution of NKT cells in both hRSV and hMPV infections. A significant decrease in the number of neutrophils, eosinophils, and CD103+DCs infiltrating to the lungs, as well as an increased production of IFN-γ, were observed upon hRSV-infection in CD1d-deficient BALB/c mice, as compared to wild-type control mice. However, this effect was not observed in the CD1d-deficient BALB/c group, upon infection with hMPV. Importantly, reduced expression of CD1d in CD11b+ DCs and epithelial cells was found in hRSV -but not hMPV-infected mice. Besides, a reduction in the expression of CD1d in alveolar macrophages of lungs from hRSV- and hMPV-infected mice was found. Such reduction of CD1d expression interfered with NKT cells activation, and consequently IL-2 secretion, as characterized by in vitro experiments for both hRSV and hMPV infections. Furthermore, increased numbers of NKT cells recruited to the lungs in response to hRSV- but not hMPV-infection was detected, resulting in a reduction in the expression of IFN-γ and IL-2 by these cells. In conclusion, both hRSV and hMPV might be differently impairing NKT cells function and contributing to the immune response triggered by these viruses.Emma Rey-JuradoKaren BohmwaldNicolás M.S. GálvezDaniela BecerraSteven A. PorcelliLeandro J. CarreñoAlexis M. KalergisTaylor & Francis Grouparticlehuman respiratory syncytial virushuman metapneumoviruspulmonary inflammationviral infectionnatural killer t cellsInfectious and parasitic diseasesRC109-216ENVirulence, Vol 11, Iss 1, Pp 580-593 (2020)
institution DOAJ
collection DOAJ
language EN
topic human respiratory syncytial virus
human metapneumovirus
pulmonary inflammation
viral infection
natural killer t cells
Infectious and parasitic diseases
RC109-216
spellingShingle human respiratory syncytial virus
human metapneumovirus
pulmonary inflammation
viral infection
natural killer t cells
Infectious and parasitic diseases
RC109-216
Emma Rey-Jurado
Karen Bohmwald
Nicolás M.S. Gálvez
Daniela Becerra
Steven A. Porcelli
Leandro J. Carreño
Alexis M. Kalergis
Contribution of NKT cells to the immune response and pathogenesis triggered by respiratory viruses
description Human respiratory syncytial virus (hRSV) and human metapneumovirus (hMPV) cause acute respiratory tract infections in children worldwide. Natural killer T (NKT) cells are unconventional T lymphocytes, and their TCRs recognize glycolipids bound to the MHC-I-like molecule, CD1d. These cells modulate the inflammatory response in viral infections. Here, we evaluated the contribution of NKT cells in both hRSV and hMPV infections. A significant decrease in the number of neutrophils, eosinophils, and CD103+DCs infiltrating to the lungs, as well as an increased production of IFN-γ, were observed upon hRSV-infection in CD1d-deficient BALB/c mice, as compared to wild-type control mice. However, this effect was not observed in the CD1d-deficient BALB/c group, upon infection with hMPV. Importantly, reduced expression of CD1d in CD11b+ DCs and epithelial cells was found in hRSV -but not hMPV-infected mice. Besides, a reduction in the expression of CD1d in alveolar macrophages of lungs from hRSV- and hMPV-infected mice was found. Such reduction of CD1d expression interfered with NKT cells activation, and consequently IL-2 secretion, as characterized by in vitro experiments for both hRSV and hMPV infections. Furthermore, increased numbers of NKT cells recruited to the lungs in response to hRSV- but not hMPV-infection was detected, resulting in a reduction in the expression of IFN-γ and IL-2 by these cells. In conclusion, both hRSV and hMPV might be differently impairing NKT cells function and contributing to the immune response triggered by these viruses.
format article
author Emma Rey-Jurado
Karen Bohmwald
Nicolás M.S. Gálvez
Daniela Becerra
Steven A. Porcelli
Leandro J. Carreño
Alexis M. Kalergis
author_facet Emma Rey-Jurado
Karen Bohmwald
Nicolás M.S. Gálvez
Daniela Becerra
Steven A. Porcelli
Leandro J. Carreño
Alexis M. Kalergis
author_sort Emma Rey-Jurado
title Contribution of NKT cells to the immune response and pathogenesis triggered by respiratory viruses
title_short Contribution of NKT cells to the immune response and pathogenesis triggered by respiratory viruses
title_full Contribution of NKT cells to the immune response and pathogenesis triggered by respiratory viruses
title_fullStr Contribution of NKT cells to the immune response and pathogenesis triggered by respiratory viruses
title_full_unstemmed Contribution of NKT cells to the immune response and pathogenesis triggered by respiratory viruses
title_sort contribution of nkt cells to the immune response and pathogenesis triggered by respiratory viruses
publisher Taylor & Francis Group
publishDate 2020
url https://doaj.org/article/59c574c9a2d5419cafa11db90d74d562
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