dc.contributor.author
Chen, Yuling
dc.contributor.author
Gaber, Timo
dc.date.accessioned
2021-09-10T11:22:07Z
dc.date.available
2021-09-10T11:22:07Z
dc.identifier.uri
https://refubium.fu-berlin.de/handle/fub188/31921
dc.identifier.uri
http://dx.doi.org/10.17169/refubium-31652
dc.description.abstract
Oxygen availability varies throughout the human body in health and disease. Under physiological conditions, oxygen availability drops from the lungs over the blood stream towards the different tissues into the cells and the mitochondrial cavities leading to physiological low oxygen conditions or physiological hypoxia in all organs including primary lymphoid organs. Moreover, immune cells travel throughout the body searching for damaged cells and foreign antigens facing a variety of oxygen levels. Consequently, physiological hypoxia impacts immune cell function finally controlling innate and adaptive immune response mainly by transcriptional regulation via hypoxia-inducible factors (HIFs). Under pathophysiological conditions such as found in inflammation, injury, infection, ischemia and cancer, severe hypoxia can alter immune cells leading to dysfunctional immune response finally leading to tissue damage, cancer progression and autoimmunity. Here we summarize the effects of physiological and pathophysiological hypoxia on innate and adaptive immune activity, we provide an overview on the control of immune response by cellular hypoxia-induced pathways with focus on the role of HIFs and discuss the opportunity to target hypoxia-sensitive pathways for the treatment of cancer and autoimmunity.
en
dc.rights.uri
https://creativecommons.org/licenses/by/4.0/
dc.subject.ddc
600 Technik, Medizin, angewandte Wissenschaften::610 Medizin und Gesundheit::610 Medizin und Gesundheit
dc.title
Hypoxia/HIF Modulates Immune Responses
dc.type
Wissenschaftlicher Artikel
dcterms.bibliographicCitation.articlenumber
260
dcterms.bibliographicCitation.doi
10.3390/biomedicines9030260
dcterms.bibliographicCitation.journaltitle
Biomedicines
dcterms.bibliographicCitation.number
3
dcterms.bibliographicCitation.originalpublishername
MDPI AG
dcterms.bibliographicCitation.volume
9
refubium.affiliation
Charité - Universitätsmedizin Berlin
refubium.resourceType.isindependentpub
no
dcterms.accessRights.openaire
open access
dcterms.bibliographicCitation.pmid
33808042
dcterms.isPartOf.eissn
2227-9059