tetano
Editor, Senior Moderator
Eur J Immunol. 2018 May 15. doi: 10.1002/eji.201747421. [Epub ahead of print]
[h=1]T cells and ILC2s are major effector cells in influenza-induced exacerbation of allergic airway inflammation in mice.[/h] W S Li B[SUP]1[/SUP], J W de Bruijn M[SUP]1[/SUP], Lukkes M[SUP]1[/SUP], van Nimwegen M[SUP]1[/SUP], M Bergen I[SUP]1[/SUP], KleinJan A[SUP]1[/SUP], H GeurtsvanKessel C[SUP]2[/SUP], Andeweg A[SUP]2[/SUP], F Rimmelzwaan G[SUP]2[/SUP], W Hendriks R[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] 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[SUP]+[/SUP] 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 na?ve 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[SUP]high[/SUP] ICOS[SUP]high[/SUP] KLRG1[SUP]high[/SUP] CD25[SUP]high[/SUP] 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. This article is protected by copyright. All rights reserved.
[h=4]KEYWORDS:[/h] Allergic airway inflammation; Allergy; Exacerbation; ILC2; Influenza virus
PMID: 29762870 DOI: 10.1002/eji.201747421
[h=1]T cells and ILC2s are major effector cells in influenza-induced exacerbation of allergic airway inflammation in mice.[/h] W S Li B[SUP]1[/SUP], J W de Bruijn M[SUP]1[/SUP], Lukkes M[SUP]1[/SUP], van Nimwegen M[SUP]1[/SUP], M Bergen I[SUP]1[/SUP], KleinJan A[SUP]1[/SUP], H GeurtsvanKessel C[SUP]2[/SUP], Andeweg A[SUP]2[/SUP], F Rimmelzwaan G[SUP]2[/SUP], W Hendriks R[SUP]1[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] 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[SUP]+[/SUP] 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 na?ve 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[SUP]high[/SUP] ICOS[SUP]high[/SUP] KLRG1[SUP]high[/SUP] CD25[SUP]high[/SUP] 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. This article is protected by copyright. All rights reserved.
[h=4]KEYWORDS:[/h] Allergic airway inflammation; Allergy; Exacerbation; ILC2; Influenza virus
PMID: 29762870 DOI: 10.1002/eji.201747421