title: Activated CD8+ T-lymphocytes in obstructive sleep apnoea.
abstract: T-lymphocytes are implicated in the development of atherosclerosis. The aim of this study was to assess whether the CD8+ T-lymphocytes of obstructive sleep apnoea (OSA) patients undergo phenotypic and functional changes that may exaggerate atherogenic sequelae in OSA. A total of 36 OSA patients, 17 controls and 15 single-night-treated OSA patients were studied. Phenotype and cytotoxicity against K562 target cells were analysed by flow cytometry. Cytotoxicity against human umbilical vein endothelial cells (HUVECs) was assessed by 51Cr release assay. The cytotoxicity of the CD8+ T-lymphocytes of OSA patients against K562 and HUVECs was significantly greater than controls. This increased cytotoxicity directly depended on the presence of perforin and natural killer receptors (CD56, CD16), which were significantly increased in OSA CD8+ T-lymphocytes. Also the percentage of the CD56bright subset, which mediates initial interactions with vascular endothelium, significantly increased in OSA. Nasal continuous positive airway pressure treatment significantly decreased CD8+ T-cell cytotoxicity and CD56 expression, and was positively correlated with natural killer inhibitory NKB1 receptor expression either after a single-night treatment or after a prolonged treatment. In conclusion, the CD8+ T-lymphocytes of obstructive sleep apnoea patients undergo phenotypic and functional changes, rendering them cytotoxic to target cells via increased CD56+/perforin+ expression, which can be ameliorated by nasal continuous positive airway pressure treatment. These results are compatible with the current authors' hypothesis of atherogenic sequelae in obstructive sleep apnoea.
authors.affiliation: The Lloyd Rigler Sleep Apnea Research Laboratory, Unit of Anatomy and Cell Biology, Techion-Israel Institute of Technology, Haifa, Israel.
authors.forename: L
authors.initials: L
authors.lastname: Dyugovskaya
authors.forename: P
authors.initials: P
authors.lastname: Lavie
authors.forename: M
authors.initials: M
authors.lastname: Hirsh
authors.forename: L
authors.initials: L
authors.lastname: Lavie
mesh_terms: D015415:Biomarkers / Q000378:metabolism; D019002:CD56 Antigen; D018414:CD8-Positive T-Lymphocytes / Q000378:metabolism*; D045422:Continuous Positive Airway Pressure; D003601:Cytotoxicity Tests, Immunologic; D042783:Endothelial Cells / Q000378:metabolism; D005260:Female; D006801:Humans; D016130:Immunophenotyping; D008213:Lymphocyte Activation / Q000276:immunology; D008297:Male; D008562:Membrane Glycoproteins / Q000378:metabolism; D008875:Middle Aged; D054353:Perforin; D052899:Pore Forming Cytotoxic Proteins; D017452:Receptors, IgG; D011971:Receptors, Immunologic / Q000378:metabolism; D054340:Receptors, KIR; D054341:Receptors, KIR3DL1; D020181:Sleep Apnea, Obstructive / Q000276:immunology* / Q000378:metabolism* / Q000628:therapy; D014471:Umbilical Veins / Q000166:cytology / Q000378:metabolism
chemical_list: D015415:Biomarkers; D019002:CD56 Antigen; D008562:Membrane Glycoproteins; D052899:Pore Forming Cytotoxic Proteins; D017452:Receptors, IgG; D011971:Receptors, Immunologic; D054340:Receptors, KIR; D054341:Receptors, KIR3DL1; D054353:Perforin