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Blood, 1 March 2004, Vol. 103, No. 5, pp. 1595-1601. Prepublished online as a Blood First Edition Paper on October 30, 2003; DOI 10.1182/blood-2003-05-1643. This Article Full Text Full Text (PDF) All Versions of this Article: 2003-05-1643v1 103/5/1595    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 Scandella, E. Articles by Groettrup, M. Search for Related Content PubMed PubMed Citation Articles by Scandella, E. Articles by Groettrup, M. Related Collections Immunobiology Phagocytes Cell Adhesion and Motility Signal Transduction Chemokines, Cytokines, and Interleukins Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  CHEMOKINES CCL19/CCL21-triggered signal transduction and migration of dendritic cells requires prostaglandin E2 Elke Scandella, Ying Men, Daniel F. Legler, Silke Gillessen, Ladislav Prikler, Burkhard Ludewig, and Marcus Groettrup From the Departments of Research, Oncology, and Urology, Cantonal Hospital St Gallen, Switzerland; and the Department of Immunology, Faculty of Biology, University of Constance, Konstanz, Germany. The control of dendritic cell (DC) migration is pivotal for the initiation of cellular immune responses. When activated with inflammatory stimuli, the chemokine receptor CCR7 is up-regulated on DCs. Activated DCs home to lymphoid organs, where the CCR7 ligands CCL19 and CCL21 are expressed. We previously found that human monocyte-derived DCs (MoDCs) exclusively migrated to CCL19 and CCL21 when matured in the presence of prostaglandin (PG) E2. Because PGE2 did not alter CCR7 cell surface expression, we examined whether PGE2 may exert its effect by coupling CCR7 to signal transduction modules. Indeed, stimulation with CCR7 ligands led to enhanced phosphatidylinositol-3-kinase–mediated phosphorylation of protein kinase B when MoDCs were matured in the presence of PGE2. Moreover, CCL19/CCL21-induced intracellular calcium mobilization in MoDCs occurred only when PGE2 was present during maturation. MoDC migration to CCL19 and CCL21 was dependent on phospholipase C and intracellular calcium flux but not on phosphatidylinositol-3 kinase. Hence, our data provide insight into CCL19/CCL21-triggered signal transduction pathways and identify a novel function for PGE2 in controlling the migration of mature MoDCs by facilitating CCR7 signal transduction. 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