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Published ahead of print on April 30, 2003, doi:10.1164/rccm.200210-1226OC

Am. J. Respir. Crit. Care Med., Volume 168, Number 2, July 2003, 242-249

A more recent version of this article appeared on July 15, 2003
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Submitted on October 27, 2002
Accepted on April 28, 2003

Phenotypic and functional characterization of blood {gamma}{delta} T cells in sleep apnea

Larissa Dyugovskaya1, Peretz Lavie1, and Lena Lavie1*

1 Faculty of Medicine, Lloyd Rigler Sleep Apnea Research Laboratory, Unit of Anatomy and Cell Biology, Technion-Israel Institute of Technology, Haifa, Israel

* To whom correspondence should be addressed. E-mail: lenal{at}tx.technion.ac.il.

Hypoxia-induced lymphocyte dysfunction may be implicated in endothelial cell damage in obstructive sleep apnea syndrome (OSA). {gamma}{delta}T cells unique migration, cytotoxic features and accumulation in atherosclerotic plaques are considered critical in cardiovascular disorders. We characterized the phenotype, cytokine profile, adhesion properties and cytotoxicity of {gamma}{delta} T cells in OSA patients and controls. The following is a summary of our major findings with regard to OSA {gamma}{delta} T cells: (1) A significant increase in the expression of the inhibitory NKB1 receptors was found (2) The intracellular content of pro-inflammatory cytokines TNF-{alpha} and IL-8 was increased, and the content of the anti-inflammatory cytokine IL-10 was decreased (3) {gamma}{delta} T cells of OSA patients adhered significantly more avidly to non-activated endothelial cells in culture than those of controls (4) L-selectin expression was higher (5) Anti-L-selectin antibodies and anti-TNF-{alpha} antibodies decreased the adhesion index of OSA {gamma}{delta} T lymphocytes/endothelial cells but not of controls (6) Cytotoxicity of OSA {gamma}{delta} T lymphocytes against endothelial cells in culture was 2.5-fold higher than controls, and could be prevented by pretreatment with anti-TNF-{alpha}. Collectively these data implicate {gamma}{delta} T lymphocyte function in atherogenic sequelae in OSA.
Key words: cytokines, adhesion, cytotoxicity, hypoxia/reperfusion, atherosclerosis




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