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Interleukin-18/interferon-gamma-inducing factor, a novel cytokine, up-regulates ICAM-1 (CD54) expression in KG-1
H Kohka1, T Yoshino, H Iwagaki
1First Department of Surgery, Okayama University School of Medicine, Shikata, Japan.
Insights
Interferon-gamma-inducing factor (IGIF), now known as IL-18, up-regulates Intercellular Adhesion Molecule-1 (ICAM-1) expression in immune cells. This IL-18 function is independent of interferon-gamma and may influence immune cell infiltration.
Area of Science:
- Immunology
- Cell Biology
- Molecular Biology
Background:
- Intercellular Adhesion Molecule-1 (ICAM-1, CD54) is a key immune response molecule.
- ICAM-1 is a ligand for Leukocyte Function-Associated Antigen-1 (LFA-1).
Purpose of the Study:
- To investigate the effect of Interferon-gamma-Inducing Factor (IGIF), proposed as IL-18, on ICAM-1 expression.
- To determine the role of IL-18 in immune cell interactions and regulation.
Main Methods:
- Utilized KG-1 cells, a human myelomonocytic cell line.
- Assessed ICAM-1 expression and cell aggregation.
- Employed blocking antibodies against ICAM-1, LFA-1, and interferon-gamma.
Main Results:
- IL-18 selectively up-regulated ICAM-1 expression in KG-1 cells.
- IL-18 induced heterotypic aggregation between KG-1 and Peer T cells, blocked by anti-ICAM-1/LFA-1 antibodies.
- ICAM-1 up-regulation by IL-18 was independent of interferon-gamma.
Conclusions:
- IL-18 enhances ICAM-1 expression and function through an interferon-gamma-independent pathway.
- IL-18 may play a role in immunoregulation by promoting immune cell infiltration.
Abstract:
Intercellular adhesion molecule-1 (ICAM-1, CD54) is a membrane glycoprotein and a member of the immunoglobulin superfamily. It plays a central role in cell to cell-mediated immune responses and is a ligand for leukocyte function-associated antigen-1 (LFA-1). We report here that a newly discovered cytokine, interferon-gamma-inducing factor (IGIF) [H. Okamura et al. (1995) Nature 378, 88] recently proposed to be designated as IL-18, selectively up-regulates ICAM-1 expression in KG-1 cells, a human myelomonocytic cell line, in which IL-18 also enhances interferon-gamma production. IL-18 induced heterotypic aggregation between KG-1 and Peer T cells, which was blocked by anti-ICAM-1 and/or LFA-1 antibodies. Anti-interferon-gamma antibody did not block the IL-18-induced up-regulation of ICAM-1 on KG-1 cells. These results thus show that IGIF/IL-18, enhances ICAM-1 expression in KG-1 cells in an interferon-gamma-independent pathway, up-regulates ICAM-1 functions, and that IL-18 might play a potential role in immunoregulation by mediating immune cell infiltration into the tissues.
