SEARCH:   Advanced

Blood, 15 December 2008, Vol. 112, No. 13, pp. 4971-4980. Prepublished online as a Blood First Edition Paper on September 25, 2008; DOI 10.1182/blood-2008-05-158469. This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: blood-2008-05-158469v1 112/13/4971    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 LeibundGut-Landmann, S. Articles by Reis e Sousa, C. Search for Related Content PubMed PubMed Citation Articles by LeibundGut-Landmann, S. Articles by Reis e Sousa, C. Related Collections Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Stimulation of dendritic cells via the dectin-1/Syk pathway allows priming of cytotoxic T-cell responses Salomé LeibundGut-Landmann1, Fabiola Osorio1, Gordon D. Brown2, and Caetano Reis e Sousa1 1 Immunobiology Laboratory, Cancer Research UK, London Research Institute, Lincoln's Inn Fields Laboratories, London, United Kingdom; and 2 Institute of Infectious Disease and Molecular Medicine, University of Cape Town, Rondebosch, South Africa The C-type lectin receptor dectin-1 functions as a pattern recognition receptor for β-glucans and signals via Syk kinase but independently of the Toll-like receptor (TLR) pathway to regulate expression of innate response genes. Dectin-1 signaling can promote activation of dendritic cells (DCs), rendering them competent to prime Th1 and Th17 responses. Here we show that dectin-1–activated DCs can also prime cytotoxic T-lymphocyte (CTL) responses. DCs exposed to a dectin-1 agonist induced antigen-specific expansion of TCR transgenic CD8+ T cells and their differentiation into CTLs in vitro. Dectin-1 agonist also acted as an adjuvant for CTL crosspriming in vivo, eliciting potent CTL responses that protected mice from tumor challenge. In vitro but not in vivo, CTL crosspriming was dependent on IL-12 p70, which was produced by dectin-1–activated DCs in response to IFN- secreted by newly activated CD8+ T cells. The dectin-1/Syk pathway is thus able to couple innate immune recognition of β-glucans to all branches of the adaptive immune system, including CD4+ T-helper cells, B cells, and CD8+ cytotoxic T cells. These data highlight the ability of non-TLR receptors to bridge innate and adaptive immunity and suggest that dectin-1 agonists may constitute useful adjuvants for immunotherapy and vaccination. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: A. Rivera, N. Collins, M. T. Stephan, L. Lipuma, I. Leiner, and E. G. Pamer Aberrant Tissue Localization of Fungus-Specific CD4+ T Cells in IL-10-Deficient Mice J. Immunol., July 1, 2009; 183(1): 631 - 641. [Abstract] [Full Text] [PDF] H. Huang, G. R. Ostroff, C. K. Lee, J. P. Wang, C. A. Specht, and S. M. Levitz Distinct Patterns of Dendritic Cell Cytokine Release Stimulated by Fungal {beta}-Glucans and Toll-Like Receptor Agonists Infect. Immun., May 1, 2009; 77(5): 1774 - 1781. [Abstract] [Full Text] [PDF]

	Copyright © 2008 by American Society of Hematology         Online ISSN: 1528-0020