Mice deficient in the IL-33 receptor ST2 are susceptible to infection with the protozoan parasite Toxoplasma gondii, but how IL-33 promotes resistance to infection remains elusive. Previous reports have attributed this susceptibility to aberrant skewing of the immune response away from type 2 immunity, with which ST2 has been classically associated, toward an excessive type 1 response and consequent lethal immune pathology in the central nervous system (CNS). Although expression of ST2 by tissue-resident Tregs supports a possible deficiency in immune regulation, ST2-knockout mice were also found to have higher parasite burdens in the CNS, suggesting a potential defect in the inflammatory response. In recent years, a direct role for IL-33/ST2 in enhancing type 1 responses has been appreciated, leading us to reconsider the function of IL-33 in the response to T. gondii. Using whole organ in vitro antigen recall assays of spleen, bone marrow, and brain tissues, we found that addition of exogenous IL-33 to Soluble Toxoplasma Antigen (STAg)-restimulated cultures enhanced interferon gamma production during both acute and chronic infection. Further, we observed that IL-33 enhanced the proliferation and differentiation of restimulated parasite-specific CD4+ and CD8+ effector T cells in vitro. To confirm the physiological relevance of our system, we used IL-33 reporter mice to confirm in vivo expression of IL-33 in intact tissues relevant to T. gondii infection, including the meninges and cervical lymph nodes. As IL-33 is expressed at high levels in many tissues, including the central nervous system, and is released during tissue damage caused by infections such as T. gondii, these results suggest that IL-33 enhances the inflammatory response to T. gondii and consequently control of this parasitic infection.