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Journal of Biomedicine and Biotechnology
Volume 2010 (2010), Article ID 795210, 11 pages
Research Article

Immune Modulation by Schistosoma mansoni Antigens in NOD Mice: Effects on Both Innate and Adaptive Immune Systems

Department of Pathology, University of Cambridge, Tennis Court Road, CB2 1QP Cambridge, UK

Received 2 September 2009; Accepted 10 November 2009

Academic Editor: Luis I. Terrazas

Copyright © 2010 Paola Zaccone et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


We have shown that Schistosoma mansoni egg soluble antigen (SEA) prevents diabetes in the nonobese diabetic (NOD) mouse inducing functional changes in antigen presenting cells (APCs) and expanding T helper (Th) 2 and regulatory T cell (Treg) responses. A Th2 response to S. mansoni infection or its antigens is key to both the establishment of tolerance and successfully reproduction in the host. More recently we demonstrated that SEA treatment upregulates bioactive TGF on T cells with consequent expansion of Tregs, and these cells might be important in SEA-mediated diabetes prevention together with Th2 cells. In this study we profile further the phenotypic changes that SEA induces on APCs, with particular attention to cytokine expression and markers of macrophage alternative activation. Our studies suggest that TGF from T cells is important not just for Treg expansion but also for the successful Th2 response to SEA, and therefore, for diabetes prevention in the NOD mouse.