Abstract
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 TGFβ on T cells with consequent expansion of Foxp3+ 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 TGFβ 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.
Highlights
Helminths employ a range of immunomodulatory strategies to modulate the host immune response and utilize it to extend their longevity in the host and facilitate transmission
Most studies in mice have been carried out using bone marrow derived antigen presenting cells (APCs) and it could be argued that it would be more relevant to examine the effect of S. mansoni antigens on isolated splenic dendritic cells (DCs) as well as in vivo on macrophage (MΦ) populations
In the absence of additional TLR stimuli, we have shown that small consistent phenotypic changes occur when DCs are stimulated in vitro
Summary
Helminths employ a range of immunomodulatory strategies to modulate the host immune response and utilize it to extend their longevity in the host and facilitate transmission. In the case of bone marrow derived DCs, it has been shown that exposure to S. mansoni antigens results in DC retention of a more immature phenotype while inducing them to mediate a Th2 response in vivo [5, 10]. Most studies in mice have been carried out using bone marrow derived APCs and it could be argued that it would be more relevant to examine the effect of S. mansoni antigens on isolated splenic DCs as well as in vivo on macrophage (MΦ) populations In this manuscript we have addressed in detail the effect of SEA on functional and phenotypic changes in DCs and MΦs and the impact that this might have on the development of different T cell subpopulations including Tregs. This presents another interesting way in which the Th1 response could be modulated as it has been suggested that excess
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