Journal
EUROPEAN JOURNAL OF IMMUNOLOGY
Volume 39, Issue 4, Pages 1098-1107Publisher
WILEY
DOI: 10.1002/eji.200838871
Keywords
Foxp3(+) Treg cells; NOD mice; Schistosoma mansoni antigens; TGF-beta; Type 1 diabetes
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Funding
- BBSRC
- Herchel Smith Fellowship
- BBSRC [BB/D522903/1] Funding Source: UKRI
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Schistosoma mansoni soluble egg antigens (SEA) profoundly regulate the infected host's immune system. We previously showed that SEA prevents type 1 diabetes in NOD mice and that splenocytes from SEA-treated mice have reduced ability to transfer diabetes to NOD.scid recipients. To further characterize the mechanism of diabetes prevention we examined the cell types involved and showed that CD25(+) T-cell depletion of splenocytes from SEA-treated donors restored their ability to transfer diabetes. Furthermore, SEA treatment increased the number and proportional representation of Foxp3(+) T cells in the pancreas of NOD mice. We have used in vitro systems to analyze the effect of SEA on the development of NOD Foxp3(+) T cells. We find that SEA can induce Foxp3 expression in naive T cells in a TGF-beta-dependent manner. Foxp3 induction requires the presence of DC, which we also show are modified by SEA to upregulate C-type lectins, IL-10 and IL-2. Our studies show that SEA can have a direct effect on CD4(+) T cells increasing expression of TGF-beta, integrin beta 8 and galectins. These effects of SEA on DC and T cells may act in synergy to induce Foxp3(+) Treg in the NOD mouse.
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