Sepsis expands a CD39
A2aR
B cells
CD39
IL-10
adenosine
immunosuppression
macrophages
plasmablast
sepsis
Journal
Immunity
ISSN: 1097-4180
Titre abrégé: Immunity
Pays: United States
ID NLM: 9432918
Informations de publication
Date de publication:
14 09 2021
14 09 2021
Historique:
received:
05
08
2020
revised:
14
09
2020
accepted:
06
08
2021
pubmed:
3
9
2021
medline:
10
11
2021
entrez:
2
9
2021
Statut:
ppublish
Résumé
Sepsis results in elevated adenosine in circulation. Extracellular adenosine triggers immunosuppressive signaling via the A2a receptor (A2aR). Sepsis survivors develop persistent immunosuppression with increased risk of recurrent infections. We utilized the cecal ligation and puncture (CLP) model of sepsis and subsequent infection to assess the role of adenosine in post-sepsis immune suppression. A2aR-deficient mice showed improved resistance to post-sepsis infections. Sepsis expanded a subset of CD39
Identifiants
pubmed: 34473957
pii: S1074-7613(21)00335-6
doi: 10.1016/j.immuni.2021.08.005
pii:
doi:
Substances chimiques
Adora2a protein, mouse
0
Antigens, CD
0
Receptor, Adenosine A2A
0
Apyrase
EC 3.6.1.5
CD39 antigen
EC 3.6.1.5
Adenosine
K72T3FS567
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
2024-2041.e8Informations de copyright
Copyright © 2021 Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of interests The authors declare no competing interests.