Infection with parasitic worms (helminths) is strongly associated with the induction of a type 2 immune response, which is beneficial for the host by controlling parasite numbers, reducing inflammation and repairing damage caused by tissue migrating parasites. Macrophages with a distinct type 2 expression profile and are found in high numbers at the site of helminth infection, but also in non-infectious settings such as tissue injury. The infectious agent, the host genotype and the local site of infection/injury, together dictate the macrophage phenotype and whether the increase in macrophage numbers is due predominantly to proliferation of resident cells or recruitment of monocytes from the blood. A major product of macrophages at the site of helminth infection is the chitinase-like protein YM1. The Allen Lab recently discovered an unexpected relationship between YM1 and IL-17, a highly inflammatory cytokine, associated with many autoimmune diseases. Using helminth models, the lab aims to understand the complex relationship between IL-17 and type 2 immunity and unravel how type 2 immune responses regulate tissue repair.