Allergic asthma is characterized by chronic airway inflammation and hyperreactivity and is thought to be mediated by an adaptive T helper‐2 ( T h2) cell‐type immune resp‐onse. Here, we demonstrate that type 2 pulmonary innate lymphoid cells ( ILC 2s) significantly contribute to production of the key cytokines IL ‐5 and IL ‐13 in experimental asthma. In naive mice, lineage‐marker negative ILC 2s expressing IL ‐7Rα, CD 25, S ca‐1, and T 1/ ST 2(IL‐33R) were present in lungs and mediastinal lymph nodes ( M ed LN s), but not in broncho‐alveolar lavage ( BAL ) fluid. Upon intranasal administration of IL ‐25 or IL ‐33, an asthma phenotype was induced, whereby ILC 2s accumulated in lungs, M ed LN s, and BAL fluid. After IL ‐25 and IL ‐33 administration, ILC 2s constituted ∼50 and ∼80% of IL ‐5 + / IL ‐13 + cells in lung and BAL , respectively. Also in house dust mite‐induced or ovalbumin‐induced allergic asthma, the ILC 2 population in lung and BAL fluid increased significantly in size and ILC 2s were a major source of IL‐5 or IL‐13. Particularly in OVA ‐induced asthma, the contribution of ILC 2s to the total population of intracellular IL‐5 + and IL‐13 + cells in the lung was in the same range as found for T h2 cells. We conclude that both ILC 2s and T h2 cells produce large amounts of IL ‐5 and IL ‐13 that contribute to allergic airway inflammation.

Pulmonary innate lymphoid cells are major producers of IL‐5 and IL‐13 in murine models of allergic asthma