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Phenotype and Functional Characterization of blood γδ T cells in Sleep Apnoea

Hypoxia induced lymphocyte dysfunction may be implicated in endothelial cell damage in Obstructive Sleep Apnoea, (OSA), in γδ T cell 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 γδ T cells in patients with OSA and control subjects.

The following is a summary of our major findings regarding OSA γδ T cells;

1. Significant increase in expression of the inhibitory natural killer B1 receptors was found.
2. The intra-cellular content of pro-inflammatory cytokines, Tumour Necrosis Factor (TNF)-ά and interlukine-8 was increased and the content of anti-inflammatory cytokine interleukin-10 was decreased.
3. δγ T cells of patients with OSA adhered significantly more to non-activated endothelial cells in culture than those of control subjects.
4. L-Selectin was higher.
5. Anti-E/P Selectin antibodies and anti-TNFά antibodies decreased the adhesion index of OSA γδ T lymphocyte/endothelial cells in culture but not of control subjects.
6. Cytotoxicity of OSA γδ T Lymphocytes against endothelial cells in culture was 2.5 times higher than that of control subjects and could be prevented by pre-treatment with anti-TNF-δ. Collectively these data implicate γδ T Lymphocyte function in arthrogenic sequlae in OSA.

Summary; This means that when the Oxygen levels drop, particularly in frequent short bursts, there is an increase in ‘‘unhelpful chemistry’. The balance of cytokines changes.  The helpful ones (10) are decreased and the dangerous ones (8) are increased along with an increase in  the ability to stick to the artery wall and to create plaque The body does have defences against this adhesion through Anti-TNF, but this is also suppressed leaving the endothelial artery lining cells vulnerable to attack by T Lymphocytes.

This then is the link between OSA and heart disease.
This is most likely at the core of the relationship between OSA and refractory hypertension.

Sleep Apnoea Syndrome: A possible contributing factor to Resistant Hypertension.

Petrez Lavie and Victor Hoffstein.  MD

Conclusions:   Our results demonstrate that hypertensive patients with sleep apnoea, whose blood pressure responds beneficially to treatment, have significantly less severe sleep apnoea than those patients whose blood pressure remains elevated despite antihypertensive therapy. Since neither obesity nor nocturnal hypoxemia appear to be important determinants of ineffective treatment, we suggest that resistant hypertension may be caused by frequent intermittent sympathetic stimulation.