Journal of Leukocyte Biology
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Originally published online as doi:10.1189/jlb.0604358 on October 21, 2004

Published online before print October 21, 2004
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(Journal of Leukocyte Biology. 2005;77:52-58.)
© 2005 by Society for Leukocyte Biology

T cell contact-mediated activation of respiratory burst in human polymorphonuclear leukocytes is inhibited by high-density lipoproteins and involves CD18

Philippe Cettour-Rose*, Thi Xuan Khanh Nguyen*, Lena Serrander{dagger}, Marie-Thérèse Kaufmann*, Jean-Michel Dayer*, Danielle Burger* and Pascale Roux-Lombard*,1

* Division of Immunology and Allergy, Department of Internal Medecine and
{dagger} Biology of Ageing Laboratory and Department of Geriatrics, University Hospital, Geneva, Switzerland

1 Correspondence: Division of Immunology and Allergy, University Hospital, 24 rue Micheli-du-Crest, 1211 Geneva 14, Switzerland. E-mail: pascale.roux-lombard{at}hcuge.ch

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.

Key Words: oxidative metabolism • lymphocyte activation • neutrophil




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A. Scanu, N. Molnarfi, K. J. Brandt, L. Gruaz, J.-M. Dayer, and D. Burger
Stimulated T cells generate microparticles, which mimic cellular contact activation of human monocytes: differential regulation of pro- and anti-inflammatory cytokine production by high-density lipoproteins
J. Leukoc. Biol., April 1, 2008; 83(4): 921 - 927.
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