The IL-33/ST2 axis has been implicated in host–parasiteinteractions during T. cruzi infection.In vitro, IL-33 stimulation of J774 macrophage-like cells enhancesTNF, IL-17, and CCL2 production while reducing intracellular parasiteburden. Moreover, cells from patientswith CD across different clinical forms display IL-33 expression,highlighting a potential role for this pathway in parasite-inducedinflammation. More recently, Boccardoand colleagues elegantly demonstratedthat the progression of T. cruzi infectionis marked by a decline in IL-33 levels. The gene discussed is IL33; the disease is Cowden disease.