Cytokine-induced enhancement of ICAM-1 expression results in increased vulnerability of tumor cells to monocyte-mediated lysis

• Published in: The Journal of immunology (1950) Vol. 146; no. 10; pp. 3682 - 3686
• Main Authors: Webb, DS, Mostowski, HS, Gerrard, TL
• Format: Journal Article
• Language: English
• Published: Bethesda, MD Am Assoc Immnol 15-05-1991; American Association of Immunologists
• Subjects: Antibodies, Monoclonal - immunology; Biological and medical sciences; Cell Adhesion Molecules - biosynthesis; Cell Adhesion Molecules - immunology; Cytokines - pharmacology; Cytotoxicity, Immunologic; General aspects (metabolism, cell proliferation, established cell line...); Humans; Intercellular Adhesion Molecule-1; Lymphocyte Function-Associated Antigen-1 - physiology; Medical sciences; Monocytes - immunology; Neoplasms - immunology; Tumor cell; Tumor Cells, Cultured; Tumors; Up-Regulation; Human; Cytolysis; Monocyte; Cytokine; Melanoma; Cell adhesion molecule; Biological marker; Cell surface; Regulation(control); Cell line; Sensitivity resistance; Tumor necrosis factor; Interleukin 1; Interferon; Tumor cell
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.146.10.3682

Pretreatment of the human melanoma cell line, A375, and the human colon carcinoma cell line, HT-29, with certain cytokines was found to increase the vulnerability of these cells to monocyte-mediated killing. This activity was found to correlate with increased expression of intercellular adhesion molecule-1 (ICAM-1) on the tumor cells and was blocked by anti-ICAM-1 antibodies. Both IFN-gamma and TNF induced large increases in the ICAM-1 expression on both cell lines and increased the susceptibility of the tumor cells to monocyte-mediated killing. IFN-alpha and IL-1 beta, however, induced only small increases in ICAM-1 expression and enhanced the lysis of the A375 cells but not the HT-29 cells by monocytes. These differences may be the result of a higher basal expression of ICAM-1 found on the A375 cells when compared with the HT-29 cells. These data indicate that regulation of ICAM-1 expression on tumor cells can alter the vulnerability of these cells to lysis by monocytes.