Allergic asthma is caused by Th2-cell-type cytokines in response to allergen exposure. Type 2 innate lymphoid cells (ILC2s) are a newly identified subset of immune cells that, along with Th2 cells, contribute to the pathogenesis of asthma by producing copious amounts of IL-5 and IL-13, which cause eosinophilia and airway hyperreactivity (AHR), a cardinal feature of asthma. ILC2s express ICOS, a T cell costimulatory molecule with a currently unknown function. Here we showed that a lack of ICOS on murine ILC2s and blocking the ICOS:ICOS-ligand interaction in human ILC2s reduced AHR and lung inflammation. ILC2s expressed both ICOS and ICOS-ligand, and the ICOS:ICOS-ligand interaction promoted cytokine production and survival in ILC2s through STAT5 signaling. Thus, ICOS:ICOS-ligand signaling pathway is critically involved in ILC2 function and homeostasis. Display omitted •Human and murine ILC2s express both ICOS and ICOS-ligand•The ICOS:ICOS-ligand interaction is required for survival and efficient function of ILC2s•STAT5 signaling is impaired in the absence of ICOS Akbari and colleagues show the requirement of Inducible T cell Costimulator (ICOS) for the survival and efficient cytokine production of type 2 innate lymphoid cells (ILC2s), which are key players in the pathogenesis of allergic asthma.