TIGIT: NEW IMMUNE CHECKPOINT IN OBSTRUCTIVE SLEEP APNOEA [Comunicación premiada]

Obstructive sleep apnoea (OSA) is a syndrome characterized by the partial or complete obstruction of the upper airways during sleep, leading to intermittent hypoxia among others conditions. These physiological disturbances are associated with an increased risk of various diseases, such as cardiovascular disease and cancer. In fact, the prevalence of cancer in individuals with OSA is 1.53 times higher than in patients without OSA. This increase could be due to the disruption of immune surveillance caused by the effect of certain immune checkpoints (IC) on T cells. One of this IC is TIGIT, an inhibitory receptor expressed in lymphocytes that interacts with the ligands CD155 and CD112, which are present on antigen-presenting and tumor cells. The binding of this receptor to its ligands downregulated T cell functions. Thus, we aim to explore TIGIT and its ligands expression on lymphocytes and monocytes respectively of patients with OSA, assessing the role of intermittent hypoxia in this context. This study includes a cohort of patients with and without OSA who underwent a sleep study. We explore TIGIT, CD155 and CD112 expression from OSA patients and control subjects and the role of intermittent hypoxia with in vitro models. We obtained these results through flow cytometry and qPCR. Our findings show that TIGIT expression in lymphocyte T membrane is upregulated in patients with severe OSA and correlates with parameters indicating OSA severity, suggesting an association between OSA and TIGIT expression. Finally, in vitro model data suggested intermittent hypoxia were associated with upregulation of TIGIT in patients with severe OSA. In patients with obstructive sleep apnea (OSA), TIGIT overexpression on the T cell membrane is mediated by intermittent hypoxia via activation of hypoxia-inducible factor 1-alpha (HIF-1α).