Interleukin-10 inhibits tumor necrosis factor-α production in lipopolysaccharide-stimulated RAW 264.7 cells through reduced MyD88 expression

Jargalsaikhan Dagvadorj, Yoshikazu Naiki, Gantsetseg Tumurkhuu, Ferdaus Hassan, Shamima Islam, Naoki Koide, Isamu Mori, Tomoaki Yoshida, Takashi Yokochi

研究成果: Article査読

25 被引用数 (Scopus)

抄録

The mechanism of interleukin (IL)-10-mediated inhibition of tumor necrosis factor (TNF)-α production was studied by lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage cells. IL-10 inhibited TNF-α production transiently at an early stage after LPS stimulation. IL-10 inhibited the activation of nuclear factor (NF)-κB, p38 and stress-activated protein kinase (SAPK) in LPS-stimulated RAW 264.7 cells. Although the level of MyD88 protein increased in response to LPS, IL-10 prevented the LPS-induced MyD88 augmentation. There was no significant difference in the MyD88 mRNA expression between the cells pretreated with or without IL-10 in response to LPS. Therefore, IL-10 was suggested to inhibit LPS-induced TNF-α production via reduced MyD88 expression.

本文言語English
ページ(範囲)109-115
ページ数7
ジャーナルInnate Immunity
14
2
DOI
出版ステータスPublished - 04-2008
外部発表はい

All Science Journal Classification (ASJC) codes

  • Microbiology
  • Immunology
  • Molecular Biology
  • Cell Biology
  • Infectious Diseases

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