ILC2s represent the predominant early source of IL-13 and IL-5 to promote and induce the development of Th2-type adaptive immune response including host resistance against parasitic helminth, airway inflammation, and airways hyperreactivity in a murine model of allergic asthma and are essential in the repair of damaged respiratory tissue following acute infection with influenza virus [12, 19–24]. This evidence concerns the gene IL5 and allergic asthma.