Tim-3 is a potential regulator that inhibits monocyte inflammation in response to intermittent hypoxia in children with obstructive sleep apnea syndrome.
Hepatitis A Virus Cellular Receptor 2
/ genetics
Humans
Hypoxia
/ pathology
Inflammation
/ immunology
Intercellular Adhesion Molecule-1
/ blood
Interleukin-12 Subunit p35
/ blood
Interleukin-6
/ blood
Monocytes
/ metabolism
Signal Transduction
Sleep Apnea, Obstructive
/ pathology
Vascular Endothelial Growth Factor A
/ blood
Inflammation
Intermittent hypoxia (IH)
Monocytes
OSAS
Tim-3
Journal
Clinical immunology (Orlando, Fla.)
ISSN: 1521-7035
Titre abrégé: Clin Immunol
Pays: United States
ID NLM: 100883537
Informations de publication
Date de publication:
01 2021
01 2021
Historique:
received:
28
06
2020
revised:
23
11
2020
accepted:
25
11
2020
pubmed:
4
12
2020
medline:
17
6
2021
entrez:
3
12
2020
Statut:
ppublish
Résumé
The mechanism of the characteristic intermittent hypoxia (IH) of obstructive sleep apnea syndrome (OSAS) on monocyte remain unclear. Our study found that OSAS children had a significantly upregulated expression in circulating proinflammatory cytokines IL-6 and IL-12, and endothelial injury markers VEGF and ICAM1. Association analysis revealed that the plasma TNFα, IL-1β, IL-6, IL-10 and IL-12 concentration were negatively associated with the minimal SpO
Identifiants
pubmed: 33271370
pii: S1521-6616(20)30801-9
doi: 10.1016/j.clim.2020.108641
pii:
doi:
Substances chimiques
HAVCR2 protein, human
0
Hepatitis A Virus Cellular Receptor 2
0
ICAM1 protein, human
0
IL12A protein, human
0
IL6 protein, human
0
Interleukin-12 Subunit p35
0
Interleukin-6
0
VEGFA protein, human
0
Vascular Endothelial Growth Factor A
0
Intercellular Adhesion Molecule-1
126547-89-5
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
108641Informations de copyright
Copyright © 2020. Published by Elsevier Inc.