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

J Leukoc Biol. 2005 Jan;77(1):52-8. doi: 10.1189/jlb.0604358. Epub 2004 Oct 21.

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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • CD18 Antigens / metabolism*
  • Cell Adhesion
  • Cell Communication / immunology
  • Cells, Cultured
  • Humans
  • Lipoproteins, HDL / metabolism*
  • Lymphocyte Activation / immunology*
  • Neutrophils / immunology*
  • Reactive Oxygen Species
  • Respiratory Burst*
  • T-Lymphocytes / physiology*

Substances

  • CD18 Antigens
  • Lipoproteins, HDL
  • Reactive Oxygen Species