Research in the Tait Wojno laboratory studies how immune responses and inflammation are regulated during helminth infection and allergic disease. Intestinal helminth parasite infection and allergic disease affect billions of humans worldwide, causing significant morbidity. Following helminth infection, mammals mount a Type 2 inflammatory response that is host-protective and helps to expel parasites and repair parasite-induced tissue damage. Allergic disease features a similar Type 2 immune response that causes pathological inflammation in response to environmental allergens. Type 2 inflammation is characterized by activation of innate immune cells, including basophils and innate lymphoid cells, the polarization of CD4+ T cells to the T helper Type 2 (Th2) fate, and production of Type 2 cytokines. These immune cell activities direct changes to epithelial cell function that result in increased mucus secretion and epithelial cell turnover, leading to worm expulsion during helminth infection or pathological inflammation during allergy. Current paradigms emphasize the role of cytokines in these events, but other biochemical factors and cell-cell interactions regulate immune and epithelial gene transcription and cellular function during infection and allergy.