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  • Title: T cell contact-mediated activation of respiratory burst in human polymorphonuclear leukocytes is inhibited by high-density lipoproteins and involves CD18.
    Author: Cettour-Rose P, Nguyen TX, Serrander L, Kaufmann MT, Dayer JM, Burger D, Roux-Lombard P.
    Journal: J Leukoc Biol; 2005 Jan; 77(1):52-8. PubMed ID: 15498815.
    Abstract:
    Polymorphonuclear neutrophils (PMN) are recruited to sites of inflammation, where they are in close vicinity with other immune cell types. The present study demonstrates that direct cell-cell contact with stimulated T cells activates PMN respiratory burst. To discard interferences with soluble products, membranes isolated from human T lymphocytes (msT) or the monocytic cell line HUT-78 (msHUT) were used to mimic cellular contact. msT and msHUT induced a dose-dependent production of radical oxygen species (ROS) in PMN, as detected by chemiluminescence. Similar results were obtained with fixed, stimulated T cells, confirming that ROS production was a result of cell-surface molecules and not to soluble products of T cells. ROS production was mainly intracellular, suggesting that ROS may take part in intracellular processes. High-density lipoproteins (HDL), which had previously been shown to inhibit T cell contact-induced cytokine production in monocyte-macrophages, potently reduced ROS production induced in PMN upon contact with stimulated T cells. This supports the emerging role of HDL as immunomodulators in inflammatory diseases. Furthermore, monoclonal antibodies to CD18 inhibited 60% of the PMN respiratory burst induced by msT, suggesting that CD18 contributed to PMN activation. The present results emphasize the importance of direct cell-cell contact with stimulated T cells in inflammatory processes.
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