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

Autor: Li BWS; Department of Pulmonary Medicine, Erasmus MC Rotterdam, Rotterdam, the Netherlands., de Bruijn MJW; Department of Pulmonary Medicine, Erasmus MC Rotterdam, Rotterdam, the Netherlands., Lukkes M; Department of Pulmonary Medicine, Erasmus MC Rotterdam, Rotterdam, the Netherlands., van Nimwegen M; Department of Pulmonary Medicine, Erasmus MC Rotterdam, Rotterdam, the Netherlands., Bergen IM; Department of Pulmonary Medicine, Erasmus MC Rotterdam, Rotterdam, the Netherlands., KleinJan A; Department of Pulmonary Medicine, Erasmus MC Rotterdam, Rotterdam, the Netherlands., GeurtsvanKessel CH; Department of Viroscience, Erasmus MC Rotterdam, Rotterdam, the Netherlands., Andeweg A; Department of Viroscience, Erasmus MC Rotterdam, Rotterdam, the Netherlands., Rimmelzwaan GF; Department of Viroscience, Erasmus MC Rotterdam, Rotterdam, the Netherlands., Hendriks RW; Department of Pulmonary Medicine, Erasmus MC Rotterdam, Rotterdam, the Netherlands.
Jazyk: angličtina
Zdroj: European journal of immunology [Eur J Immunol] 2019 Jan; Vol. 49 (1), pp. 144-156. Date of Electronic Publication: 2018 Jun 11.
DOI: 10.1002/eji.201747421
Abstrakt: 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.
(© 2018 The Authors. European Journal of Immunology published by WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)
Databáze: MEDLINE
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