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Sulfatide binding and activation of leukocytes through an L-selectin-independent pathway.

Journal of Leukocyte Biology

Animals, Antibodies, Monoclonal, pharmacology, Antigens, CD18, physiology, Antigens, CD29, Binding Sites, Cations, Divalent, Cattle, Cell Adhesion, drug effects, Cell Aggregation, Cells, Cultured, Consensus Sequence, Culture Media, Culture Media, Serum-Free, Dogs, Endothelium, Vascular, cytology, Enzyme Inhibitors, Fetal Blood, Intercellular Adhesion Molecule-1, Jugular Veins, L-Selectin, Leukocytes, Lymph Nodes, Lymphocyte Function-Associated Antigen-1, Lymphoma, pathology, Male, Molecular Weight, Neoplasm Proteins, Protein Kinase C, Protein-Tyrosine Kinases, Rats, Rats, Wistar, Receptors, Cell Surface, chemistry, isolation & purification, metabolism, Signal Transduction, Tumor Cells, Cultured, Specific Pathogen-Free Organisms, Sulfoglycosphingolipids, T-Lymphocytes, Tetradecanoylphorbol Acetate

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      Abstract

      Sulfatide has been reported to activate leukocytes through L-selectin. Here we provide evidence that sulfatide binds to and activates leukocytes through both L-selectin-dependent and -independent pathways. Rat leukocytes of various sources shed surface L-selectin after phorbol myristate acetate (PMA) treatment, however, these cells retained the ability to bind sulfatide. In addition, sulfatide also bound to an L-selectin-negative cell line EL-4, and the binding was up-regulated by PMA. Sulfatide induced aggregation of L-selectin-positive lymphocytes, which was highly dependent on divalent cations, protein tyrosine kinases (PTK), and protein kinase C (PKC), but was independent of beta1 and beta2 integrins. In contrast, sulfatide-induced EL-4 cell aggregation required an LFA-1/ICAM-1 adhesion pathway but not PTK and PKC. A sulfatide receptor of 65 kDa was isolated from EL-4 cells. Taken together, this study suggests that sulfatide can bind to and activate leukocytes through an L-selectin-independent molecule and triggers signal transduction pathways different from those induced by L-selectin activation.

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