Nature Immunology
1, 353 - 357 (2000)
doi:10.1038/79815
DC-SIGN−ICAM-2 interaction mediates dendritic cell traffickingTeunis B. H. Geijtenbeek1, Daniëlle J. E. B. Krooshoop1, 3, Diederik A. Bleijs1, 3, Sandra J. van Vliet1, Gerard C. F. van Duijnhoven1, Valentine Grabovsky2, Ronen Alon2, Carl G. Figdor1
& Yvette van Kooyk11
Department of Tumor Immunology, University Medical Center St Radboud, Philips van Leydenlaan 25, Nijmegen 6525 EX, The Netherlands. 2
Department of Immunology, The Weizmann Institute of Science, Rehovot 76100, Israel. 3
These authors contributed equally to this work.
Correspondence should be addressed to Yvette van Kooyk Y.vanKooyk@dent.kun.nlDendritic cells (DCs) are recruited from blood into tissues to patrol for foreign antigens. After antigen uptake and processing, DCs migrate to the secondary lymphoid organs to initiate immune responses. We now show that DC-SIGN, a DC-specific C-type lectin, supports tethering and rolling of DC-SIGN−positive cells on the vascular ligand ICAM-2 under shear flow, a prerequisite for emigration from blood. The DC-SIGN−ICAM-2 interaction regulates chemokine-induced transmigration of DCs across both resting and activated endothelium. Thus, DC-SIGN is central to the unusual trafficking capacity of DCs, further supported by the expression of DC-SIGN on precursors in blood and on immature and mature DCs in both peripheral and lymphoid tissues.
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