Abstract
The expression of intercellular adhesion molecule-1 (ICAM-1) on primary human fibroblasts, a human fibrosarcoma, chondrosarcoma, and adenocarcinoma cell line in response to IL-1, TNF-alpha, or IFN-gamma was studied using an ELISA with anti-ICAM-1 mAb. The induction of ICAM-1 by these cytokines was neutralized by cytokine-specific antisera as well as some steroids and the glycosylation inhibitor, tunicamycin. Cyclohexamide up-regulated the expression of ICAM-1 on chondrosarcoma cells but had little or no effect on carcinoma cells. These data indicate different mechanisms in the regulation and expression of ICAM-1 on the various cell types and provide some insight into the anti-inflammatory effects of some pharmacologic agents.
MeSH terms
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Animals
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Antibodies, Monoclonal / physiology*
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Antigens, Surface / antagonists & inhibitors
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Antigens, Surface / biosynthesis*
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Biological Products / antagonists & inhibitors
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Biological Products / immunology
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Biological Products / pharmacology*
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Cell Adhesion Molecules
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Cell Line
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Cytokines
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Humans
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Immune Sera / pharmacology*
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Inflammation / etiology
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Inflammation / immunology*
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Interferon-gamma / immunology
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Interferon-gamma / pharmacology
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Interleukin-1 / immunology
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Interleukin-1 / pharmacology
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Kinetics
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Mice
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Neutralization Tests
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Rabbits
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Tumor Necrosis Factor-alpha / immunology
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Tumor Necrosis Factor-alpha / pharmacology
Substances
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Antibodies, Monoclonal
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Antigens, Surface
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Biological Products
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Cell Adhesion Molecules
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Cytokines
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Immune Sera
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Interleukin-1
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Tumor Necrosis Factor-alpha
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Interferon-gamma