T cells and ILC2s are major effector cells in influenza-induced exacerbation of allergic airway inflammation in mice.
Eur J Immunol
; 49(1): 144-156, 2019 01.
Article
em En
| MEDLINE
| ID: mdl-29762870
ABSTRACT
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/ST2high ICOShigh KLRG1high CD25high 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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Base de dados:
MEDLINE
Assunto principal:
Orthomyxoviridae
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Sistema Respiratório
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Linfócitos
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Infecções por Orthomyxoviridae
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Células Th2
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Fator de Transcrição GATA3
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Influenza Humana
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Hipersensibilidade
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Inflamação
Idioma:
En
Ano de publicação:
2019
Tipo de documento:
Article
País de afiliação:
Holanda