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Vol. 60. Issue 4.
Pages 207-214 (April 2024)
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Vol. 60. Issue 4.
Pages 207-214 (April 2024)
Original Article
Dysregulation in CD39/CD73 Axis May Trigger the Upsurge of the Immune Suppressive Agent Adenosine in OSA Patients
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Elena Díaz-Garcíaa,b, Aldara García-Sáncheza,c, Enrique Alfaroa,b,d, Cristina López-Fernándeza,b, Eva Mañasc, Raquel Casitasb, Sara Vegab, Irene Cano-Pumaregac, Francisco García-Ríoa,b,d,
Corresponding author
fgr01m@gmail.com

Corresponding authors.
, Carolina Cubillos-Zapataa,b,
Corresponding author
cubilloszapata@gmail.com

Corresponding authors.
a Biomedical Research Networking Centre on Respiratory Diseases (CIBERES), Madrid, Spain
b Respiratory Diseases Group, Respiratory Diseases Department, La Paz University Hospital, IdiPAZ, Madrid, Spain
c Servicio de Neumología, Hospital Universitario Ramón y Cajal, Madrid, Spain
d Faculty of Medicine, Autonomous University of Madrid, Madrid, Spain
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Table 1. Main Characteristics of Study Subjects.
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Abstract
Introduction

Although higher incidence of cancer represents a major burden for obstructive sleep apnea (OSA) patients, the molecular pathways driving this association are not completely understood. Interestingly, adenosinergic signaling has emerged as a powerful immune checkpoint driving tumor development and progression.

Methods

Here, we explored the expression of the adenosinergic ecto-enzymes CD39 and CD73 in T-lymphocytes of OSA patients without any evidence of cancer, as well as their soluble forms in plasma (sCD39 and sCD73), along with adenosine. In addition, we explored the role of intermittent hypoxia (IH) in this context by in vitro models.

Results

Our results showed that CD39 is upregulated while CD73 is downregulated in OSA T-cells’ membrane. Moreover, our findings suggest that IH, through HIF-1, mediates the upregulation of both CD39 and CD73; and that CD73 downregulation could be mediated by a higher release of sCD73 by OSA T-lymphocytes. Importantly, we found that both sCD39 and sCD73 are upregulated in OSA plasma, suggesting T-lymphocytes as a potential source for plasmatic sCD73. Finally, our data propose the alterations in CD39/CD73 axis could underlie the upsurge of adenosine levels in the plasma of OSA patients.

Conclusion

Our study reveals a hypoxia-mediated alteration of the CD39/CD73 axis in OSA patients, which could trigger ADO upregulation, thus potentially contributing to the immune suppressive environment and ultimately facilitating tumor development and progression. Therefore, our data highlights the need for new longitudinal studies evaluating CD39 and/or CD73 as potential cancer-risk prognostic biomarkers in OSA patients.

Keywords:
Sleep apnea
Intermittent hypoxia
CD39
CD73
Adenosine
Immunosuppression
Abbreviations:
OSA
HIF-1α
IH
PD-1/PD-L1
PSGL-1
ADO
ATP
AMP
NK
CS
AHI
SaO2
PBMCs
PX-478
DMOG
IL-
IFN
TNF
TGF-β
STAT
EVs

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