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Mediators of Inflammation
Volume 2013, Article ID 312590, 7 pages
Research Article

Plasmacytoid Dendritic Cell Response to CpG ODN Correlates with CXCL16 Expression and Is Inhibited by ox-LDL

1Department of Biological Sciences, Middle East Technical University, 06800 Ankara, Turkey
2Cancer and Inflammation Program, National Cancer Institute, Frederick, MD 21702, USA
3Department of Molecular Biology and Genetics, Bilkent University, 06800 Ankara, Turkey

Received 16 July 2013; Accepted 6 September 2013

Academic Editor: Ishak Tekin

Copyright © 2013 Mayda Gursel 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.


Structurally distinct classes of synthetic CpG oligonucleotides (ODN) differentially activate human immune cells. K-type ODN trigger plasmacytoid dendritic cells (pDCs) to differentiate and produce TNFα. In contrast, D-type ODN stimulate large amounts of IFNα secretion from pDCs. The cell-surface receptor CXCL16 was previously shown to influence the nature and specificity of CpG ODN-induced immune activation. Here, we evaluated the expression and function of CXCL16 on pDC from healthy volunteers. We report that increased CXCL16 expression correlated with enhanced in vitro response exclusively to D-type CpG ODN. Conversely, enzymatic digestion of the receptor resulted in a decrease in IFNα production. Moreover, ox-LDL presence significantly inhibited D-ODN mediated IFNα production by pDCs. Coculture of enriched pDCs with the CXCR6 expressing Jurkat T cells decreased the activation threshold of these cells responding to D-ODN, suggesting that CXCL16/CXCR6 interaction may play an important role in modifying the response of pDCs to environmental danger signals.