ToxSci Advance Access published online on February 18, 2003
Toxicological Sciences, doi:10.1093/toxsci/kfg012
Toxicological Sciences © Society of Toxicology 2003; all rights reserved
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1 Department of Environmental and Molecular Toxicology and Environmental Health Sciences Center, Oregon State University, Corvallis, OR 97331, USA
* To whom correspondence should be addressed. E-mail: nancy.kerkvliet{at}orst.edu.
We have previously shown that exposure of mice to TCDD induces activation-like changes in splenic dendritic cells (DC) in the absence of antigen challenge. Since activation of DC reduces their ability to phagocytize antigen, the effects of TCDD on the ability of DC to process and present antigen to antigen-specific T cells and to internalize latex beads were examined. Additionally, the expression of costimulatory and adhesion molecules was examined on DC from TCDD-treated mice injected with allogeneic tumor cells. The ability of DC from C57Bl/6 mice to induce proliferation of KLH-specific 10.5.17 T cells and production of IL-4 was not significantly altered by TCDD exposure, either when KLH was added in vitro or when the mice were injected with KLH prior to DC isolation. In contrast, OVA presentation by DC from TCDD-treated Balb/c mice induced enhanced proliferation of OVA-specific D011.10 T cells, although the production of IL-2 and IFN-
© 2003 Society of Toxicology
Immunotoxicology
Influence of 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) on the Antigen-Presenting Activity of Dendritic Cells
Abstract 
was not affected. Enhanced in vivo proliferation of adoptively transferred, CFSE-labeled DO11.10 T cells was also observed in TCDD-treated Balb/c mice that were challenged with OVA. TCDD treatment modulated the expression of MHC class II, CD24, ICAM-1, CD40, and LFA-1 on splenic DC from C57Bl/6 mice injected with allogeneic tumor cells, however the effects of TCDD were identical to changes seen previously in nonimmune mice, suggesting that these effects were not antigen-dependent. Finally, TCDD treatment did not affect the ability of splenic DC to internalize latex beads administered in vivo. Taken together, these results suggest that the activation-like changes induced in DC by TCDD do not suppress the ability of DC to process and present antigen, but may enhance their ability to provide activation signals to T cells. This, in turn, may alter the survival of the T cells, the DC, or both, and lead to dysregulation of the immune response.
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