Neutrophil Signaling That Challenges Dogmata of G Protein-Coupled Receptor Regulated Functions.
Journal
ACS pharmacology & translational science
ISSN: 2575-9108
Titre abrégé: ACS Pharmacol Transl Sci
Pays: United States
ID NLM: 101721411
Informations de publication
Date de publication:
10 Apr 2020
10 Apr 2020
Historique:
received:
09
01
2020
entrez:
17
4
2020
pubmed:
17
4
2020
medline:
17
4
2020
Statut:
epublish
Résumé
Activation as well as recruitment of neutrophils, the most abundant leukocyte in human blood, to sites of infection/inflammation largely rely on surface-exposed chemoattractant receptors. These receptors belong to the family of 7-transmembrane domain receptors also known as G protein-coupled receptors (GPCRs) due to the fact that part of the downstream signaling relies on an activation of heterotrimeric G proteins. The neutrophil GPCRs share significant sequence homologies but bind many structurally diverse activating (agonistic) and inhibiting (antagonistic) ligands, ranging from fatty acids to purines, peptides, and lipopeptides. Recent structural and functional studies of neutrophil receptors have generated important information on GPCR biology in general; this knowledge aids in the overall understanding of general pharmacological principles, governing regulation of neutrophil function and inflammatory processes, including novel leukocyte receptor activities related to ligand recognition, biased/functional selective signaling, allosteric modulation, desensitization mechanisms and reactivation, and communication (cross-talk) between GPCRs. This review summarizes the recent discoveries and pharmacological hallmarks with focus on neutrophil GPCRs. In addition, unmet challenges are dealt with, including recognition by the receptors of diverse ligands and how biased signaling mediates different biological effects.
Identifiants
pubmed: 32296763
doi: 10.1021/acsptsci.0c00004
pmc: PMC7155189
doi:
Types de publication
Journal Article
Review
Langues
eng
Pagination
203-220Informations de copyright
Copyright © 2020 American Chemical Society.
Déclaration de conflit d'intérêts
The authors declare no competing financial interest.
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