In addition to the human studies, in the Gazzinelli Lab we use mouse models to assess the functional consequences of the interaction between allergen- and helminth-driven type-2 immune responses, and to investigate the impact of the cross-reactivity between House Dust Mite (HDM)- and helminth-antigens in the allergic effector response, as well as in the mediated host resistance to helminths. Recently, investigating the interface between Ascaris infection (the most prevalence helminth worldwide) and pulmonary allergic inflammation induced by HDM, we identified Ascaris-encoded tropomyosin and enolase as the two major HDM homologues based on high sequence and structural similarity (Gazzinelli-Guimaraes et al., 2021). We showed that the HDM-triggered IgE cross-reactive antibodies that were functional as they mediated immediate hypersensitivity responses in skin testing. We also demonstrated that helminth tropomyosin was capable of inducing a severe type-2 associated pulmonary inflammation following the sensitization with the homologous house dust mite tropomyosin (Der p 10). These findings suggested a potential underlying mechanism to explain how helminth infections induce or exacerbate allergic inflammation.