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T cells and ILC2s are major effector cells in influenza‐induced exacerbation of allergic airway inflammation in mice

Influenza virus infection is an important cause of severe asthma exacerbations, but it remains unclear how a Th1‐mediated antiviral response triggers a prototypical Th2 disease. We investigated CD4(+) T cells and group 2 innate lymphoid cells (ILC2s) in influenza virus‐infected mice. We found that I...

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Autores principales: Li, Bobby W. S., de Bruijn, Marjolein J. W., Lukkes, Melanie, van Nimwegen, Menno, Bergen, Ingrid M., KleinJan, Alex, GeurtsvanKessel, Corine H., Andeweg, Arno, Rimmelzwaan, Guus F., Hendriks, Rudi W.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6585726/
https://www.ncbi.nlm.nih.gov/pubmed/29762870
http://dx.doi.org/10.1002/eji.201747421
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author Li, Bobby W. S.
de Bruijn, Marjolein J. W.
Lukkes, Melanie
van Nimwegen, Menno
Bergen, Ingrid M.
KleinJan, Alex
GeurtsvanKessel, Corine H.
Andeweg, Arno
Rimmelzwaan, Guus F.
Hendriks, Rudi W.
author_facet Li, Bobby W. S.
de Bruijn, Marjolein J. W.
Lukkes, Melanie
van Nimwegen, Menno
Bergen, Ingrid M.
KleinJan, Alex
GeurtsvanKessel, Corine H.
Andeweg, Arno
Rimmelzwaan, Guus F.
Hendriks, Rudi W.
author_sort Li, Bobby W. S.
collection PubMed
description Influenza virus infection is an important cause of severe asthma exacerbations, but it remains unclear how a Th1‐mediated antiviral response triggers a prototypical Th2 disease. We investigated CD4(+) T cells and group 2 innate lymphoid cells (ILC2s) in influenza virus‐infected mice. We found that ILC2s accumulated in the lung rapidly after influenza virus infection, but the induction of IL‐5 and IL‐13 secretion was delayed and concomitant with T cell activation. In an influenza‐induced exacerbation of allergic airway inflammation model we noticed an initial reduction of ILC2 numbers and cytokine production in broncho‐alveolar lavage compared to chronic house dust mite (HDM)‐mediated airway inflammation alone. ILC2s phenotype was characterized by low T1/ST2, ICOS, KLRG1, and CD25 expression, resembling naïve ILC2s. The contribution of ILC2s to type 2 cytokine production in the early stage of the influenza‐induced exacerbation was limited. In contrast, T cells showed increased IL‐4 and IL‐5 production when exposed to both HDM and influenza virus. Upon virus clearance, ILC2s regained an activated T1/ST2(high)ICOS(high)KLRG1(high)CD25(high) phenotype paired with cytokine production and were major contributors to the type 2 cytokine milieu. Collectively, our data indicate that both T cells and ILC2s contribute to influenza‐induced exacerbation of allergic airway inflammation, but with different kinetics.
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spelling pubmed-65857262019-06-27 T cells and ILC2s are major effector cells in influenza‐induced exacerbation of allergic airway inflammation in mice Li, Bobby W. S. de Bruijn, Marjolein J. W. Lukkes, Melanie van Nimwegen, Menno Bergen, Ingrid M. KleinJan, Alex GeurtsvanKessel, Corine H. Andeweg, Arno Rimmelzwaan, Guus F. Hendriks, Rudi W. Eur J Immunol Allergy and inflammation Influenza virus infection is an important cause of severe asthma exacerbations, but it remains unclear how a Th1‐mediated antiviral response triggers a prototypical Th2 disease. We investigated CD4(+) T cells and group 2 innate lymphoid cells (ILC2s) in influenza virus‐infected mice. We found that ILC2s accumulated in the lung rapidly after influenza virus infection, but the induction of IL‐5 and IL‐13 secretion was delayed and concomitant with T cell activation. In an influenza‐induced exacerbation of allergic airway inflammation model we noticed an initial reduction of ILC2 numbers and cytokine production in broncho‐alveolar lavage compared to chronic house dust mite (HDM)‐mediated airway inflammation alone. ILC2s phenotype was characterized by low T1/ST2, ICOS, KLRG1, and CD25 expression, resembling naïve ILC2s. The contribution of ILC2s to type 2 cytokine production in the early stage of the influenza‐induced exacerbation was limited. In contrast, T cells showed increased IL‐4 and IL‐5 production when exposed to both HDM and influenza virus. Upon virus clearance, ILC2s regained an activated T1/ST2(high)ICOS(high)KLRG1(high)CD25(high) phenotype paired with cytokine production and were major contributors to the type 2 cytokine milieu. Collectively, our data indicate that both T cells and ILC2s contribute to influenza‐induced exacerbation of allergic airway inflammation, but with different kinetics. John Wiley and Sons Inc. 2018-06-11 2019-01 /pmc/articles/PMC6585726/ /pubmed/29762870 http://dx.doi.org/10.1002/eji.201747421 Text en © 2018 The Authors. European Journal of Immunology published by WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Allergy and inflammation
Li, Bobby W. S.
de Bruijn, Marjolein J. W.
Lukkes, Melanie
van Nimwegen, Menno
Bergen, Ingrid M.
KleinJan, Alex
GeurtsvanKessel, Corine H.
Andeweg, Arno
Rimmelzwaan, Guus F.
Hendriks, Rudi W.
T cells and ILC2s are major effector cells in influenza‐induced exacerbation of allergic airway inflammation in mice
title T cells and ILC2s are major effector cells in influenza‐induced exacerbation of allergic airway inflammation in mice
title_full T cells and ILC2s are major effector cells in influenza‐induced exacerbation of allergic airway inflammation in mice
title_fullStr T cells and ILC2s are major effector cells in influenza‐induced exacerbation of allergic airway inflammation in mice
title_full_unstemmed T cells and ILC2s are major effector cells in influenza‐induced exacerbation of allergic airway inflammation in mice
title_short T cells and ILC2s are major effector cells in influenza‐induced exacerbation of allergic airway inflammation in mice
title_sort t cells and ilc2s are major effector cells in influenza‐induced exacerbation of allergic airway inflammation in mice
topic Allergy and inflammation
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6585726/
https://www.ncbi.nlm.nih.gov/pubmed/29762870
http://dx.doi.org/10.1002/eji.201747421
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