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The role of tumor necrosis factor-α for interleukin-10 production by murine dendritic cells

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Title: The role of tumor necrosis factor-α for interleukin-10 production by murine dendritic cells
Authors: Hirata, Noriyuki Browse this author
Yanagawa, Yoshiki Browse this author
Ogura, Hisako Browse this author
Satoh, Masashi Browse this author
Noguchi, Masayuki Browse this author
Matsumoto, Machiko Browse this author
Togashi, Hiroko Browse this author
Onoé, Kazunori Browse this author
Iwabuchi, Kazuya Browse this author
Keywords: Dendritic cells
Interleukin-10
Signal transduction
Tumor necrosis factor-α
Toll-like receptor
Issue Date: 2011
Publisher: Elsevier
Journal Title: Cellular Immunology
Volume: 266
Issue: 2
Start Page: 165
End Page: 171
Publisher DOI: 10.1016/j.cellimm.2010.09.012
PMID: 20979991
Abstract: In the present study, we examined the role of tumor necrosis factor (TNF) in interleukin (IL)-10 production by dendritic cells (DCs) using bone-marrow derived DCs from wild type (WT) and TNF-α knockout (TNF-α^[-/-]) mice. Toll-like receptor (TLR) stimulation induced substantial level of IL-10 production by WT DCs, but significantly low level of IL-10 production by TNF-α^[-/-] DCs. In contrast, no significant difference was detected in IL-12 p40 production between WT and TNF-α^[-/-] DCs. Addition of TNF-α during TLR stimulation recovered the impaired ability of TNF-α^[-/-] DCs for IL-10 production. This recovery appeared to be associated with an activation of extracellular signal-regulated kinase, p38 mitogen-activated protein kinase, and phosphatidylinositol 3-kinase/Akt following the TNF-α addition. Blocking these kinases significantly inhibited IL-10 production by TNF-α^[-/-] DCs stimulated with TLR ligands plus TNF-α. Thus, TNF-α may be a key molecule to regulate the balance between anti-inflammatory versus inflammatory cytokine production in DCs.
Type: article (author version)
URI: http://hdl.handle.net/2115/45137
Appears in Collections:遺伝子病制御研究所 (Institute for Genetic Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 平田 徳幸

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