Background: Helminth infections, particularly S.mansoni, are known to induce a protective role against various forms of autoimmune diseases, including type 1diabetes (TID). The observed S.mansoni significant inhibition or delay of diabetes development in non-obese diabetic mice (NOD), appeared to be due to a modulation of the diabetes-associated th1response towards protective th2 responses through IL-10 production. Objective: To study the effect of S. mansoni SEA on the immune response in induced TIDmouse moduel.  Material and Methods: In this study, 90 male Swiss Albino mice of 6 weeks old, weighing between 90 and 100g were divided into 5 groups; control group (I): Streptozontocin (STZ)-treated group (II); soluble egg antigen (SEA)-immunized group (III); (STZ+SEA) group (IV); (SEA+STZ) group (V). Mice were subjected to measurement of blood glucose levels at two and four weeks by colorimetric method, and measurement of IL-10 by enzyme linked immunosorbent assay (ELISA). Histopathological examination of pancreatic sections of the five groups investigated signs suggesting presence or absence of pancreatic inflammation.   Results: Significant lowering of blood glucose level occurred at 2-weeks in groups III and V compared to group II and at 4-weeks in groups III, IV and V compared to group II, and in group V compared to group IV. Significant higher IL-10 level occurred at 2-weeks in groups IV and V compared to group II, and in groups IV and V compared to group III and in group V compared to group IV. In 4-weeks, significant increase in IL-10 level occurred in groups II, IV, V compared to group I, and in group V compared to group IV. No significant difference between groups III and I was recorded. Histopathological changes of pancreatic sections of groups I and III showed normal architecture of pancreatic cells; While groups II and IV coinciding with STZ treatment showed vacuolation and necrosis of islets of Langerhans at 2-weeks the inflammation subsided in group IV. In group V there was dilation of blood vessels with inflammatory cells at both weeks. Conclusion: S.mansoni derived SEA proved to be protective against TID leading to improvement of blood sugar control and indicating the protective role of S.mansoni infection.