Low-Dose Lipopolysaccharide Modifies the Production of IL-12 by Dendritic Cells in Response to Various Cytokines

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著者

    • SAITO Yusuke
    • Division of Immunobiology, Institute for Genetic Medicine, Hokkaido University
    • YANAGAWA Yoshiki
    • Division of Immunobiology, Institute for Genetic Medicine, Hokkaido University
    • KIKUCHI Kazuhiro
    • Division of Immunobiology, Institute for Genetic Medicine, Hokkaido University
    • IIJIMA Norifumi
    • Division of Immunobiology, Institute for Genetic Medicine, Hokkaido University
    • IWABUCHI Kazuya
    • Division of Immunobiology, Institute for Genetic Medicine, Hokkaido University
    • ONOE Kazunori
    • Division of Immunobiology, Institute for Genetic Medicine, Hokkaido University

抄録

Dendritic cell (DC) activation is triggered by cytokines, including tumor necrosis factor (TNF)-α, and microbe components, including lipopolysaccharide (LPS). During the initial stage of infection, the microbe components appear to be present at low concentration. To determine the role of low-dose microbe-components in DC activation during the initial stage of infection, we examined the effects of low-dose LPS on cytokine-induced maturation and function of DCs. Low-dose LPS (1 ng/ml) treatment of DCs had only additive effects on the expression of CD86 and major histocompatibility complex class II induced by various cytokines, including interleukin (IL)-1β, TNF-α and interferon (IFN)-γ. IL-1β alone significantly induced IL-12 production in DCs, whereas TNF-α or IFN-γ induced modest levels of IL-12 production. When low-dose LPS (1 ng/ml), which only slightly induced IL-12 production, was added to the culture, only an additive effect was seen on IL-1β-induced IL-12 production. In contrast, low-dose LPS synergistically enhanced TNF-α- or IFN-γ-induced IL-12 production. SB203580, a specific inhibitor of p38 MAPK, markedly inhibited TNF-α- or IFN-γ-induced IL-12-production either in the absence or presence of LPS, but showed only modest effects on IL-1β-induced IL-12-production. These findings suggest that the p38 MAPK pathway is essential for the synergistic IL-12 production induced by TNF-α- or IFN-γ in combination with low-dose LPS in DC.

収録刊行物

  • Journal of clinical and experimental hematopathology  

    Journal of clinical and experimental hematopathology 46(1), 31-36, 2006-03-01 

    The Japanese Society for Lymphoreticular Tissue Research

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各種コード

  • NII論文ID(NAID)
    10018113770
  • NII書誌ID(NCID)
    AA11556796
  • 本文言語コード
    ENG
  • 資料種別
    ART
  • ISSN
    13464280
  • データ提供元
    CJP書誌  J-STAGE 
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