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Blood, 1 May 2006, Vol. 107, No. 9, pp. 3617-3623. Prepublished online as a Blood First Edition Paper on January 5, 2006; DOI 10.1182/blood-2005-08-3419. This Article Full Text Full Text (PDF) All Versions of this Article: 2005-08-3419v1 107/9/3617    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Hanabuchi, S. Articles by Liu, Y.-J. Search for Related Content PubMed PubMed Citation Articles by Hanabuchi, S. Articles by Liu, Y.-J. Related Collections Immunobiology Signal Transduction Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Human plasmacytoid predendritic cells activate NK cells through glucocorticoid-induced tumor necrosis factor receptor-ligand (GITRL) Shino Hanabuchi, Norihiko Watanabe, Yi-Hong Wang, Yui-Hsi Wang, Tomoki Ito, Joanne Shaw, Wei Cao, F. Xiao-Feng Qin, and Yong-Jun Liu From the Department of Immunology and Center for Cancer Immunology Research, The University of Texas M. D. Anderson Cancer Center, Houston, TX. Plasmacytoid dendritic cell precursors (pDCs) are professional type I interferon-producing cells, a critical cell type in regulating innate and adaptive immune responses. By microarray gene expression analysis, we found that pDCs activated by virus or CpG-ODN preferentially express the ligand for the glucocorticoid-induced tumor necrosis factor receptor (GITRL), which was confirmed by reverse transcriptase-polymerase chain reaction (RT-PCR) and flow cytometry analysis. Using the same approaches, we found GITR is expressed by activated natural killer (NK) cells and T cells. We show that pDCs activated by CpG-ODN promote NK cell cytotoxicity and interferon (IFN)- production through type I IFNs and GITRL. Using a GITRL-transfected cell line, we further demonstrate that GITRL promotes NK cell cytotoxicity and IFN- production in synergy with interleukin-2 (IL-2), IFN-, and NKG2D triggering. We also demonstrated that pDCs localized in close contact to NK cells in T-cell areas of the tonsils, and a subpopulation of the pDCs expressed GITRL. This study reveals a novel function of GITR/GITRL in pDC-mediated coactivation of NK cells. 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