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Blood, 4 June 2009, Vol. 113, No. 23, pp. 5839-5847. Prepublished online as a Blood First Edition Paper on April 7, 2009; DOI 10.1182/blood-2008-10-184796. This Article Full Text Full Text (PDF) Supplemental Figures All Versions of this Article: blood-2008-10-184796v1 113/23/5839    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 CrossRef Google Scholar Articles by Jin, J.-O Articles by Kwak, J.-Y. PubMed PubMed Citation Articles by Jin, J.-O Articles by Kwak, J.-Y. Related Collections Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Ligand of scavenger receptor class A indirectly induces maturation of human blood dendritic cells via production of tumor necrosis factor- Jun-O Jin1,2, Hae-Young Park1,2, Qi Xu1,2, Joo-In Park1,2, Tatyana Zvyagintseva3, Valentin A. Stonik3, and Jong-Young Kwak1,2 1 Department of Biochemistry, School of Medicine and 2 Medical Research Center for Cancer Molecular Therapy, Dong-A University, Busan, Korea; and 3 Pacific Institute of Bioorganic Chemistry, Far East Branch of the Russian Academy of Sciences, Vladivostok, Russia Dendritic cells (DCs) are the most potent antigen-presenting cells for naive T cells. In this study, scavenger receptor class A type I and type II (SR-A) were shown to be expressed by peripheral blood DCs (PBDCs) and monocyte-derived DCs (MDDCs). In addition, the binding of anti–SR-A antibody to these cells was lower in the presence of fucoidan, an SR-A agonist. Treatment of these DCs with fucoidan or anti–SR-A antibody markedly increased the surface expression of costimulatory molecules CD83 and major histocompatibility complex class II on the CD11chighCD123low myeloid subset of PBDCs. Furthermore, fucoidan-treated PBDCs produced tumor necrosis factor- (TNF-) but not IL-12p70. In addition, fucoidan-induced maturation was eliminated by pretreatment with TNF-–neutralizing antibody. Finally, interferon- secretion and T-cell proliferation were enhanced by coculture of T cells with fucoidan-matured PBDCs. Specific inhibitors of p38 MAPK and glycogen synthase kinase 3 suppressed TNF- production and maturation of fucoidan-treated PBDCs. Moreover, MDDCs lacking SR-A failed to up-regulate CD83 expression, TNF- production, and phosphorylation of p38 MAPK and glycogen synthase kinase 3-β in the presence of fucoidan. Taken together, these results suggest that ligation of SR-A leads to induction of TNF-, which subsequently induces PBDC maturation, thereby leading to enhanced T-cell stimulatory capacity. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

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