• LiBobby W SBWDepartment of Pulmonary Medicine, Erasmus MC Rotterdam, Rotterdam, The Netherlands., Marjolein J W de Bruijn, Irma Tindemans, Melanie Lukkes, Alex KleinJan, Henk C Hoogsteden, and Rudi W Hendriks.
• Department of Pulmonary Medicine, Erasmus MC Rotterdam, Rotterdam, The Netherlands.
• Eur. J. Immunol. 2016 Jun 1; 46 (6): 1392-403.

AbstractAllergic asthma is a chronic inflammation of the airways mediated by an adaptive type 2 immune response. Upon allergen exposure, group 2 innate lymphoid cells (ILC2s) can be rapidly activated and represent an early innate source of IL-5 and IL-13. Here, we used a house dust mite (HDM)-driven asthma mouse model to study the induction of ILC2s in allergic airway inflammation. In BALF, lungs, and lymph nodes, ILC2 activation is critically dependent on prior sensitization with HDM. Importantly, T cells are required for ILC2 induction, whereby T-cell activation precedes ILC2 induction. During HDM-driven allergic airway inflammation the accumulation of ILC2s in BALF is IL-33 independent, although infiltrating ILC2s produce less cytokines in Il33(-/-) mice. Transfer of in vitro polarized OVA-specific OT-II Th2 cells alone or in combination with Th17 cells followed by OVA and HDM challenge is not sufficient to induce ILC2, despite significant eosinophilic inflammation and T-cell activation. In this asthma model, ILC2s are therefore not an early source of Th2 cytokines, but rather contribute to type 2 inflammation in which Th2 cells play a key role. Taken together, ILC2 induction in HDM-mediated allergic airway inflammation in mice critically depends on activation of T cells.© 2016 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.

30 keywords...

hide…