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Hypoxia and the regulation of myeloid cell metabolic imprinting: consequences for the inflammatory response
Author(s) -
Sadiku Pranvera,
Walmsley Sarah R
Publication year - 2019
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.15252/embr.201847388
Subject(s) - hypoxia (environmental) , myeloid cells , imprinting (psychology) , myeloid , inflammatory response , microbiology and biotechnology , inflammation , biology , genomic imprinting , chemistry , immunology , biochemistry , oxygen , gene expression , gene , dna methylation , organic chemistry
Inflamed and infected tissue sites are characterised by oxygen and nutrient deprivation. The cellular adaptations to insufficient oxygenation, hypoxia, are mainly regulated by a family of transcription factors known as hypoxia‐inducible factors ( HIF s). The protein members of the HIF signalling pathway are critical regulators of both the innate and adaptive immune responses, and there is an increasing body of evidence to suggest that the elicited changes occur through cellular metabolic reprogramming. Here, we review the literature on innate immunometabolism to date and discuss the role of hypoxia in innate cell metabolic reprogramming, and how this determines immune responses.