Interleukin-10-induced CCR5 expression in macrophage like HL-60 cells: Involvement of Erk1/2 and STAT-3

Yoko Makuta, Yoshiko Sonoda, Daisuke Yamamoto, Megumi Funakoshi-Tago, Eriko Aizu-Yokota, Yutaka Takebe, Tadashi Kasahara

Research output: Contribution to journalArticlepeer-review

18 Citations (Scopus)


As an immunosuppressive and anti-inflammatory cytokine, IL-10 was recently reported to play roles in CCR5 expression in human monocytes. CCR5 promoter regions contain Oct-2, TCF-1γ, GATA, and STAT binding sites. Here, we studied the signals involved in the CCR5 expression in IL-10-stimulated cells using the HL-60 cell line. HL-60 cells were stimulated with PMA and differentiated to macrophage-like cells, then stimulated with IL-10. IL-10 induced significant expression of CCR5 protein and CCR5 mRNA in these cells. The induction of CCR5 by IL-10 was inhibited by a MEK-1 inhibitor, PD98059. In addition, IL-10 induced tyrosine (Tyr) phosphorylation of Erk, as well as serine (Ser) and Tyr phosphorylation of STAT-3. Tyr phosphorylation of Erk and Ser phosphorylation of STAT-3 were inhibited by PD98059, while Tyr phosphorylation of STAT-3 was not inhibited by PD98059. DNA binding activity of STAT-3 was observed by the stimulation with IL-10, which was inhibited by PD98059. These results first indicate that Erk1/2 and STAT-3 regulate CCR5 expression, and that Erk-mediated phosphorylation of Ser is required for full stimulation of STAT-3 in CCR5 expression.

Original languageEnglish
Pages (from-to)1076-1081
Number of pages6
JournalBiological and Pharmaceutical Bulletin
Issue number8
Publication statusPublished - 2003 Aug


  • CCR5
  • IL-10
  • MEK inhibitor
  • STAT-3

ASJC Scopus subject areas

  • Pharmacology
  • Pharmaceutical Science


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