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Published online before print October 21, 2004

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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0604358

Received for publication June 25, 2004.
Revised September 21, 2004.
Accepted for publication September 23, 2004.

Article

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 , Marie-Thérèse Kaufmann ^*, Jean-Michel Dayer ^*, Danielle Burger ^*, and Pascale Roux-Lombard ^*@

Division of Immunology and Allergy, Departments of Internal Medecine and Biology of Ageing Laboratory and *Geriatrics, University Hospital, Geneva, Switzerland

^@ To whom correspondence should be addressed. E-mail: pascale. roux-lombard{at}hcuge.ch.

	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.

Key Words: oxidative metabolism • lymphocyte activation • neutrophil

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