Due to respiration, our lungs are in continuous contact with the surrounding environment, sampling several liters of air each minute. Despite this perpetual exposure to potential pathogens and antigens, the lungs are maintained in a quiescent, non-inflamed state. Pulmonary infection, exposure to allergens or contact with hazardous materials, however, can initiate an efficient immune response to eradicate the invading organism or particle. In the case of allergy, some individuals mount an excessive immune response, which can manifest as asthma or respiratory allergy and is to a large extent triggered by deregulated type 2 immunity and respective cytokines. T helper 2 cells and the recently identified population of group 2 innate lymphoid cells (ILC2s) are the main source of type 2 signature cytokines. Importantly, ILC2s are committed to type 2 immunity and thus able to elicit beneficial responses, but can also exhibit excessive type 2 immune activity if dysregulated. The Duerr laboratory studies the underlying mechanisms of ILC2 regulation and function during development and ontogeny with the focus on pulmonary immunity. With our work, we hope to expand the knowledge of basic research in lung immunity to facilitate the development and identification of novel therapeutic strategies to improve lung health and thereby overall life quality.