Given that primary Hp infections are not readily expelled by mice, that IgG responses appear key to expulsion during secondary infection [93], and that TH2 cells generated during Hp infection are capable of expelling Nb infection in the lungs in an IL‐33‐dependent manner, IL‐33's input into adaptive memory cell formation may contribute more to immunity than its direct stimulation of effector lymphoid cell cytokine activity in the Hp‐infected small intestine. This evidence concerns the gene IL33 and infection.