Background: Type 1 diabetes is an autoimmune illness with high Th1 response that destroys the islets ß-cells causing their death. Insulin therapy for T1D cannot prevent the damaging immune response in pancreatic tissue. This study aimed to assess the effects of S. mansoni SEA antigen on experimentally induced-T1D as an immune therapy. Methods: five groups of mice (7 mice each) have been employed; Control ve (I), STZ treated (II); SEA immunized (III), SEA STZ prophylactic (IV) and SEA STZ curative (V) groups. Biochemical data such as blood glucose, insulin level, and immunological markers such as insulin autoantibodies (IAA) and serum IL-10 level were used. Histological and immunohistochemical alterations in ß-cells have been investigated. Results: A potential immune effect of SEA in treating and preventing the development of T1D was recorded evident by lower blood glucose and higher blood insulin levels. Elevated serum IL 10 levels in both curative and preventive SEA groups compared to the STZ treated group, which had a typical pathological condition of T1D manifested as high blood glucose, low blood insulin, and a lower level of IL 10. The results of IAA levels, histological, and immunohistochemical tests in all groups were consistent with the biochemical data demonstrating an effective immunological modulatory impact of SEA on the course of T1D. Conclusion: This study contributes to the expanding body of data supporting the efficacy of S. mansoni antigens on autoimmune diabetes. More studies are needed to determine the complete immunological effect of parasitic helminths, in order to create innovative pharmacological therapies for human use.