Abstract
We demonstrated that tumour necrosis factor alpha (TNF-alpha) and interleukin 4 (IL-4) increased endothelial cell (EC) adhesiveness for peripheral blood lymphocytes (PBL) by promoting transcription and protein synthesis. The different kinetics observed with TNF-alpha and IL-4 suggest the involvement of different adhesion molecules. Blocking adhesion assays and immunofluorescence analysis showed that PBL adhesion to endothelial cells involves different pair adhesion molecules. Whereas IL-4 promoted an LFA-1-dependent/ICAM-1-independent adhesion pathway on EC, TNF-alpha stimulated an LFA-1-dependent/ICAM-1-dependent adhesion pathway on EC. In contrast, VLA-4/VCAM-1 molecules were involved in PBL adhesion both to IL-4 and to TNF-alpha-stimulated EC. Finally, we found that a CD2-dependent/LFA-3-independent adhesion pathway was mainly involved in IL-4-stimulated EC.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Antigens, CD / physiology
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Antigens, Differentiation, T-Lymphocyte / physiology
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CD2 Antigens
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CD58 Antigens
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Cell Adhesion / drug effects
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Cell Adhesion Molecules / physiology
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Cells, Cultured
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Cycloheximide / pharmacology
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Dactinomycin / pharmacology
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Endothelium, Vascular / drug effects
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Endothelium, Vascular / physiology*
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Humans
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Interleukin-4 / pharmacology*
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Lymphocyte Function-Associated Antigen-1 / physiology
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Lymphocytes / drug effects
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Lymphocytes / physiology*
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Membrane Glycoproteins / physiology
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Receptors, Immunologic / physiology
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Receptors, Very Late Antigen / physiology
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Tumor Necrosis Factor-alpha / pharmacology*
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Vascular Cell Adhesion Molecule-1
Substances
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Antigens, CD
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Antigens, Differentiation, T-Lymphocyte
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CD2 Antigens
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CD58 Antigens
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Cell Adhesion Molecules
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Lymphocyte Function-Associated Antigen-1
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Membrane Glycoproteins
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Receptors, Immunologic
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Receptors, Very Late Antigen
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Tumor Necrosis Factor-alpha
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Vascular Cell Adhesion Molecule-1
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Dactinomycin
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Interleukin-4
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Cycloheximide