Abstract
A twofold increase in lymphocyte adherence to rat microvascular endothelial cells (EC) was achieved by incubating EC for 4 h with IL-1 alpha or dibutyryl-cAMP (stimulators of protein kinase A, PKA) and PMA (stimulator of protein kinase C, PKC). Monoclonal antibodies anti-CD11a, anti-CD18 (LFA-1) and anti-CD49d (VLA-4 alpha) significantly inhibited the increased lymphocyte binding to IL-1 alpha-induced EC, anti-CD18 and to a lesser extent anti-CD11a and anti-CD49d to dibutyryl-cAMP-induced EC, whereas only anti-CD11a and anti-CD18 monoclonal antibodies inhibited PMA-induced lymphocyte binding. These findings suggest that stimulation of PKA and PKC induces lymphocyte binding to EC via different adhesion molecules.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Antigens, CD / immunology
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Bucladesine / metabolism
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CD18 Antigens
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Cell Adhesion / drug effects*
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Cell Adhesion Molecules / metabolism*
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Endothelium, Vascular / cytology*
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In Vitro Techniques
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Intercellular Adhesion Molecule-1
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Interleukin-1 / pharmacology
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Lymphocyte Function-Associated Antigen-1 / immunology
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Lymphocyte Function-Associated Antigen-1 / metabolism
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Lymphocytes / cytology*
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Protein Kinase C / physiology*
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Protein Kinases / physiology*
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Rats
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Receptors, Very Late Antigen / metabolism
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Tetradecanoylphorbol Acetate / pharmacology
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Vascular Cell Adhesion Molecule-1
Substances
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Antigens, CD
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CD18 Antigens
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Cell Adhesion Molecules
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Interleukin-1
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Lymphocyte Function-Associated Antigen-1
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Receptors, Very Late Antigen
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Vascular Cell Adhesion Molecule-1
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Intercellular Adhesion Molecule-1
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Bucladesine
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Protein Kinases
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Protein Kinase C
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Tetradecanoylphorbol Acetate