Phenotypic and Functional Characterization of Blood γδ T Cells in Sleep Apnea

The phenotype, cytokine profile, adhesion properties, and cytotoxicity of T cells in patients with OSA and control subjects are characterized and cytoxia-induced lymphocyte dysfunction may be implicated in endothelial cell damage in obstructive sleep apnea (OSA) syndrome.

Abstract

Hypoxia-induced lymphocyte dysfunction may be implicated in endothelial cell damage in obstructive sleep apnea (OSA) syndrome. gammadelta 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 gammadelta T cells in patients with OSA and control subjects. The following is a summary of our major findings regarding OSA gammadelta T cells: (1) a significant increase in the expression of the inhibitory natural killer B1 receptors was found; (2) the intracellular content of proinflammatory cytokines tumor necrosis factor (TNF)-alpha and interleukin-8 was increased, and the content of the antiinflammatory cytokine interleukin-10 was decreased; (3) gammadelta T cells of patients with OSA adhered significantly more avidly to nonactivated endothelial cells in culture than those of control subjects; (4) L-selectin expression was higher; (5) anti-E/P-selectin antibodies and anti-TNF-alpha antibodies decreased the adhesion index of OSA gammadelta T lymphocytes/endothelial cells but not of control subjects; and (6) cytotoxicity of OSA gammadelta T lymphocytes against endothelial cells in culture was 2.5-fold higher than that of control subjects and could be prevented by pretreatment with anti-TNF-alpha. Collectively these data implicate gammadelta T lymphocyte function in atherogenic sequelae in OSA.