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Prepublished online as a Blood First Edition Paper on September 22, 2003; DOI 10.1182/blood-2002-07-2322. This Article Full Text (PDF) All Versions of this Article: 2002-07-2322v1 103/2/648    most recent Alert me when this article is cited Alert me if a correction is posted 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 Kaser, A. Articles by Tilg, H. Search for Related Content PubMed PubMed Citation Articles by Kaser, A. Articles by Tilg, H. Social Bookmarking                   What's this? Submitted July 31, 2002 Accepted September 4, 2003 Interleukin-18 attracts plasmacytoid dendritic cells (DC2) and promotes Th1 induction by DC2 through IL-18 receptor expression Arthur Kaser, Susanne Kaser, Nicole C Kaneider, Barbara Enrich, Christian J Wiedermann, and Herbert Tilg* Department of Medicine, Division of Gastroenterology and Hepatology, University Hospital Innsbruck, Innsbruck, Austria Department of Medicine, Division of General Internal Medicine, University Hospital Innsbruck, Innsbruck, Austria * Corresponding author; email: Herbert.Tilg{at}uibk.ac.at. In vivo evidence suggests that interleukin-18 (IL-18) shapes the development of adaptive immunity toward T helper cell type 1 (Th1) responses. Monocyte-derived dendritic cells 1 (DC1) preferentially induce a Th1 response, while plasmacytoid DC-derived DC2 have been linked to a Th2 response. We analyzed the role of IL-18 during the initiation phase of a Th response in vitro to elucidate the basis of the aforementioned in vivo observations. IL-18 was constitutively released from DC1, but not DC2. Neutralization of IL-18 in co-culture experiments of DC1 with allogeneic naive T lymphocytes did not alter the Th1/Th2 phenotype, while anti-IL-12 efficiently downregulated the Th1 response. Unexpectedly, IL-18R and chain were expressed on DC2 lineage. IL-18R expression was functional as IL-18 induced chemotaxis in plasmacytoid DC (pre-DC2), and enhanced the allostimulatory capacity of IL-3-differentiated DC2. Pre-DC2 exposed to IL-18 skewed the development of Th cells toward Th1 in co-culture experiments of DC2 and allogeneic naive T cells, which was inhibited by IL-12 p70 neutralization. IL-18 might have a profound role during the initiation phase of an immune response by recruiting pre-DC2 and modulating the function of DC2. 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