Asthma is a chronic inflammation of the airways leading to airway hyperreactivity and bronchoconstriction in response to allergens as well as unspecific stimuli such as cold air [1]. Classically, the key player cells in the pathogenesis of asthma are known to be T helper cells subsets including Th2, Th9 and Th17 as well as iNK T cells and dendritic cells [1–3]. An important aspect of the classical model of the pathogenesis of asthma is the requirement for T cells and antigen specificity. Discovery of type 2 innate lymphoid cells (ILC2s) has substantially changed our understanding of the pathogenesis of asthma. ILC2s are a newly identified immune cells distinct from all known immune cells including T and B cells, dendritic cells, macrophages and granulocytes [4]. These new players in the pathogenesis of asthma can rapidly react to stimuli such as IL-25, IL-33 and TSLP and produce large amounts of Th2 cytokines, IL-5, IL-13 and the Th9 cytokine, IL-9 causing airway inflammation and hyperreactivity in non-antigen specific manner and independent of adaptive immunity [5]. In the T cell-mediated response, T cell receptor provides the antigen specific signal whereas costimulatory molecules provide the secondary signal to T cells resulting in an efficient T cell response. Unlike T cells, ILC2s lack any specific antigen receptor and receive activation signal mainly through cytokine stimuli, thus the expression of costimulatory molecules by ILC2s seems to be unnecessary. However, one of the hallmarks of ILC2 definition has been the expression of Inducible T cell COStimulator (ICOS) and the importance of ICOS is to the extent that it has been used as a means to specifically identify and deplete ILC2s in mice [6].