Maternal immune activation (MIA) is a pivotal risk factor for neurodevelopmental disorders, including autism spectrum disorder. However, the mechanisms of MIA at the maternal-fetal interface remain elusive. Here, we used soluble tachyzoite antigen (STAg) from Toxoplasma gondii to induce MIA in pregnant mice at E14.5, followed by maternal administration of interleukin-33 (IL-33) from E15.5 to E17.5. Proteomic profiling coupled with protein-protein interaction network analysis nominated IL-33 as a candidate immunoregulatory factor. In exploratory analyses, maternal IL-33 administration was associated with shifts in macrophage-associated immune profiles, reduced placental inflammation, and attenuated MIA-associated behavioral abnormalities in adult offspring. Given that suppression of tumorigenicity 2 (ST2) is the cognate receptor for IL-33, we next interrogated this pathway in ST2-deficient mice. ST2 deficiency abolished the effects of IL-33 on macrophage repolarization and inflammatory homeostasis, and the behavioral improvements were not evident in ST2-deficient offspring. Mechanistically, IL-33 administration was associated with reduced glycolytic features and improved mitochondrial function in macrophages, consistent with partial restoration of immunometabolic homeostasis at the maternal-fetal interface. Collectively, our findings highlight an immunometabolic axis in STAg-induced MIA pathogenesis, revealing IL-33/ST2 signaling as a potential experimental target for mitigating MIA-associated immune and behavioral abnormalities.