House dust mite-derived proteases contribute to allergic disorders in part by disrupting epithelial barrier function. Interleukin-33 (IL-33), produced by lung cells after exposure to protease allergens, can induce innate-type airway eosinophilia by activating natural helper (NH) cells, a member of group 2 innate lymphoid cells (ILC2), to secrete Th2 type-cytokines. Because IL-33 also can induce mast cells (MCs) to secrete Th2 type-cytokines, MCs are thought to cooperate with NH cells in enhancing protease or IL-33-mediated innate-type airway eosinophilia. However, we found that MC-deficient KitW-sh/W-sh mice exhibited exacerbated protease-induced lung inflammation associated with reduced numbers of regulatory T (Treg) cells. Moreover, IL-2 produced by IL-33-stimulated MCs promoted expansion of numbers of Treg cells, thereby suppressing development of papain- or IL-33-induced airway eosinophilia. We have thus identified a unique anti-inflammatory pathway that can limit induction of innate-type allergic airway inflammation mediated by NH cells. Display omitted •MC-deficient mice exhibit exacerbated papain-induced lung inflammation•Such lung inflammation is associated with reduced numbers of Treg cells•IL-2 produced by IL-33-stimulated mast cells promotes Treg cell expansion•MCs suppress papain-induced airway inflammation by numbers of Treg cells The role of mast cells (MCs) in non-Th2 cell- and non-IgE-mediated allergic disorders is unknown. Nakae and colleagues show that IL-33-stimulated MC-derived IL-2 enhances expansion of numbers of regulatory T cells, thereby suppressing of allergic inflammation.