Thus, in the current study we sought to assess the role of ILC2s in the regulation of allergen- and IL-33-induced bone marrow eosinophilia utilizing wild type (WT) mice, Rag1−/− mice lacking mature T and B cells but retain ILCs, and mice lacking all lymphocytes (Rag2−/−Il2rg−/−). The gene discussed is IL33; the disease is Increased total eosinophil count.