Tim-3 is a potential regulator that inhibits monocyte inflammation in response to intermittent hypoxia in children with obstructive sleep apnea syndrome

Tim-3 is a potential regulator that inhibits monocyte inflammation in response to intermittent hypoxia in children with obstructive sleep apnea syndrome

Copyright © 2020. Published by Elsevier Inc.

Bibliographische Detailangaben
Veröffentlicht in:Clinical immunology (Orlando, Fla.). - 1999. - 222(2021) vom: 04. Jan., Seite 108641
1. Verfasser: Wang, Wei (VerfasserIn)
Weitere Verfasser: Xu, Zhifei, Zhang, Jie, Wang, Shengcai, Ge, Wentong, Li, Xiaodan, Mou, Wenjun, Wang, Xiaolin, Chai, Wenjia, Zhao, Jing, Wang, Guixiang, Xi, Yue, Qiu, Yue, Ji, Tingting, Gui, Jingang, Tai, Jun, Ni, Xin
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2021
Zugriff auf das übergeordnete Werk:Clinical immunology (Orlando, Fla.)
Schlagworte:Journal Article Research Support, Non-U.S. Gov't Inflammation Intermittent hypoxia (IH) Monocytes OSAS Tim-3 HAVCR2 protein, human Hepatitis A Virus Cellular Receptor 2 ICAM1 protein, human mehr... IL12A protein, human IL6 protein, human Interleukin-12 Subunit p35 Interleukin-6 VEGFA protein, human Vascular Endothelial Growth Factor A Intercellular Adhesion Molecule-1 126547-89-5
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520 |a 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 SpO2, a negative index for disease severity. OSAS monocytes presented an inflammatory phenotype with higher mRNA levels of inflammatory cytokines. Importantly, we noted a significant decrease in T-cell immunoglobulin and mucin domain (Tim)-3 expression in OSAS monocytes with the increase of the plasma proinflammatory cytokines. In vitro assay demonstrated that IH induced THP-1 cell overactivation via NF-κB dependent pathway was inhibited by the Tim-3 signal. Our results indicated that activation of monocyte inflammatory responses is closely related to OSAS-induced IH, and negatively mediated by a Tim-3 signaling pathway 
650 4 |a Journal Article 
650 4 |a Research Support, Non-U.S. Gov't 
650 4 |a Inflammation 
650 4 |a Intermittent hypoxia (IH) 
650 4 |a Monocytes 
650 4 |a OSAS 
650 4 |a Tim-3 
650 7 |a HAVCR2 protein, human  |2 NLM 
650 7 |a Hepatitis A Virus Cellular Receptor 2  |2 NLM 
650 7 |a ICAM1 protein, human  |2 NLM 
650 7 |a IL12A protein, human  |2 NLM 
650 7 |a IL6 protein, human  |2 NLM 
650 7 |a Interleukin-12 Subunit p35  |2 NLM 
650 7 |a Interleukin-6  |2 NLM 
650 7 |a VEGFA protein, human  |2 NLM 
650 7 |a Vascular Endothelial Growth Factor A  |2 NLM 
650 7 |a Intercellular Adhesion Molecule-1  |2 NLM 
650 7 |a 126547-89-5  |2 NLM 
700 1 |a Xu, Zhifei  |e verfasserin  |4 aut 
700 1 |a Zhang, Jie  |e verfasserin  |4 aut 
700 1 |a Wang, Shengcai  |e verfasserin  |4 aut 
700 1 |a Ge, Wentong  |e verfasserin  |4 aut 
700 1 |a Li, Xiaodan  |e verfasserin  |4 aut 
700 1 |a Mou, Wenjun  |e verfasserin  |4 aut 
700 1 |a Wang, Xiaolin  |e verfasserin  |4 aut 
700 1 |a Chai, Wenjia  |e verfasserin  |4 aut 
700 1 |a Zhao, Jing  |e verfasserin  |4 aut 
700 1 |a Wang, Guixiang  |e verfasserin  |4 aut 
700 1 |a Xi, Yue  |e verfasserin  |4 aut 
700 1 |a Qiu, Yue  |e verfasserin  |4 aut 
700 1 |a Ji, Tingting  |e verfasserin  |4 aut 
700 1 |a Gui, Jingang  |e verfasserin  |4 aut 
700 1 |a Tai, Jun  |e verfasserin  |4 aut 
700 1 |a Ni, Xin  |e verfasserin  |4 aut 
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