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Interleukin‐18/interferon‐γ‐inducing factor, a novel cytokine, up‐regulates ICAM‐1 (CD54) expression in KG‐1 cells
Author(s) -
Kohka Hideo,
Yoshino Tadashi,
Iwagaki Hiromi,
Sakuma Isao,
Tanimoto Tadao,
Matsuo Yosinobu,
Kurimoto Masashi,
Orita Kunzo,
Akagi Tadaatsu,
Tanaka Noriaki
Publication year - 1998
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.64.4.519
Subject(s) - biology , immune system , cytokine , microbiology and biotechnology , interferon , icam 1 , antibody , interferon gamma , immunology , cell adhesion molecule
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‐γ‐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‐γ 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‐γ 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‐γ‐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. J. Leukoc. Biol . 64: 519–527; 1998.