Small Extracellular Vesicles Harboring PD-L1 in Obstructive Sleep Apnea

Author:

Recoquillon Sylvain1,Ali Sakina2,Justeau Grégoire3,Riou Jérémie4ORCID,Martinez M. Carmen5ORCID,Andriantsitohaina Ramaroson5ORCID,Gagnadoux Frédéric13ORCID,Trzepizur Wojciech13

Affiliation:

1. SFR ICAT, Team Carme, MitoVasc Laboratory, UMR CNRS 6015 INSERM 1083, University of Angers, 49000 Angers, France

2. INSERM 1063, University of Angers, 49045 Angers, France

3. Department of Respiratory and Sleep Medicine, Angers University Hospital, 49100 Angers, France

4. Delegation for Clinical Research and Innovation, Angers University Hospital, 49100 Angers, France

5. PhyMedExp, Montpellier University, INSERM, CNRS, CHRU Montpellier, 34295 Montpellier, France

Abstract

Obstructive sleep apnea syndrome (OSA) has been associated with increased cancer incidence and aggressiveness. One hypothesis to support this association is the implication of immune response, particularly the programmed cell death pathway, formed by the receptor PD-1 and its ligand PD-L1. Recent studies have shown dysregulation of this pathway in severe OSA patients. It has also been shown that small extracellular vesicles (sEVs) carrying PD-L1 induce lymphocyte dysfunction. Thus, the aim of our study was to analyze the expression of PD-L1 on sEVs of OSA patients and to evaluate the role of sEVs on lymphocyte activation and cytotoxicity. Circulating sEVs were isolated from OSA patients and the control group. Lymphocytes were isolated from the control group. Circulating sEVs were characterized by western blot, nanotracking analysis, and flow cytometry and were incubated with lymphocytes. Our results show no differences in the quantity and composition of sEVs in OSA patients and no significant effects of sEVs in OSA patients on lymphocyte activation and cytotoxicity. These results suggest that OSA does not modify PD-L1 expression on sEVs, which does not contribute to dysregulation of cytotoxic lymphocytes.

Funder

Pays de la Loire Health Research Institute

Publisher

MDPI AG

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