ILC2s are also the primary source of IL-5, another type 2 cytokine induced by IL-33 secretion, which has been shown to promote the accumulation of eosinophils and the exacerbation of disease in influenza infected lungs of mice (194), and these lung resident ILC2s contribute to the induction of an immunopathogenic type 2 response in RSV and influenza infections. The gene discussed is IL5; the disease is influenza.