IL-18-induced expression of intercellular adhesion molecule-1 in human monocytes: Involvement in IL-12 and IFN-γ production in PBMC

Atsushi Yoshida, Hideo Kohka Takahashi, Masahiro Nishibori, Hiromi Iwagaki, Tadashi Yoshino, Toshihiko Morichika, Minori Yokoyama, Eisaku Kondo, Tadaatsu Akagi, Noriaki Tanaka

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

IL-18 time- and concentration-dependently upregulated the expression of intercellular adhesion molecule-1 (ICAM-1) in a monocyte population in human PBMC as determined by FACS analysis while the expression of CD11a, CD18, CD29, CD44, and CD62L in monocytes and that of ICAM-1, CD11a, CD18, CD29, CD44, and CD62L in T cells was not influenced by IL-18. IL-18 in the same concentration range stimulated the production of IL-12, TNF-α, and IFN-γ in culture of PBMC; however, IL-18-induced expression of ICAM-1 in monocytes was not inhibited by anti-IL-12, anti-TNF-α, or anti-IFN-γ Ab, suggesting the independence of the upregulating effect of IL-18 on endogenous IL-12, TNF-α, and IFN-γ production. IL-18 also induced the aggregation of PBMC, which was prevented by anti-ICAM-1 and anti-LFA-1 Abs. On the other hand, anti-ICAM-1 and anti-LFA-1 Abs inhibited IL-18-induced production of three cytokines, IL-12, IFN-γ and TNF-α, by 60 and 40%, respectively. These results strongly suggested that the IL-18-induced upregulation of ICAM-1 and the subsequent adhesive interaction through ICAM-1 on monocytes and LFA-1 on T/NK cells generate an additional stimulatory signaling as well as an efficient paracrine environment for the IL-18-initiated cytokine cascade.

Original languageEnglish
Pages (from-to)106-115
Number of pages10
JournalCellular Immunology
Volume210
Issue number2
DOIs
Publication statusPublished - Jun 15 2001

Keywords

  • Human
  • ICAM-1
  • IFN-γ
  • IL-12
  • IL-18
  • LFA-1
  • Monocytes

ASJC Scopus subject areas

  • Immunology

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