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dc.contributor.authorKaser, A
dc.contributor.authorHosomi, Shuhei
dc.contributor.authorGrootjans, Joep
dc.contributor.authorHuang, Yu-Hwa
dc.contributor.authorBlumberg, Richard S
dc.date.accessioned2018-10-10T09:15:27Z
dc.date.available2018-10-10T09:15:27Z
dc.date.issued2018
dc.identifier.issn1664-3224
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/283494
dc.description.abstractNatural-killer group 2 member D (NKG2D) is a well-characterized activating receptor expressed by natural killer (NK) cells, NKT cells, activated CD8+ T cells, subsets of γδ+ T cells, and innate-like T cells. NKG2D recognizes multiple ligands (NKG2D-ligands) to mount an innate immune response against stressed, transformed or infected cells. NKG2D-ligand surface expression is tightly restricted on healthy cells through transcriptional and post-transcriptional mechanisms, while transformed or infected cells express the ligands as a danger signal. Recent studies have revealed that unfolded protein response (UPR) pathways during endoplasmic reticulum (ER) stress result in up-regulation of ULBP-related protein via the PERK-ATF4-CHOP pathway, which can be linked to the pathogenesis of autoimmune diseases. Transformed cells however possess mechanisms to escape NKG2D-mediated immune surveillance, such as upregulation of carcinoembryonic antigen (CEA)-related cell adhesion molecule 1 (CEACAM1), a negative regulator of NKG2D-ligands. In this review, we discuss mechanisms of NKG2D-ligand regulation, with a focus on newly discovered mechanisms that promote NKG2D-ligand expression on epithelial cells, including ER stress, and mechanisms that suppress NKG2D-ligand mediated killing of cancer cells, namely by co-expression of CEACAM1.
dc.description.sponsorshipWellcome Trust Senior Investigator Award 106260/Z/14/Z, the European Research Council HORIZON2020/ERC grant no. 648889 (A.K.)
dc.languageeng
dc.publisherFrontiers Media
dc.rightsAttribution 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectnatural-killer group 2 member D
dc.subjectnatural-killer group 2 member D-ligand
dc.subjectmurine UL16-binding protein like transcript 1
dc.subjectUL16 binding protein 1
dc.subjectendoplasmic reticulum stress
dc.subjectCEA-related cell adhesion molecule 1
dc.titleNew Insights Into the Regulation of Natural-Killer Group 2 Member D (NKG2D) and NKG2D-Ligands: Endoplasmic Reticulum Stress and CEA-Related Cell Adhesion Molecule 1
dc.typeArticle
prism.number1324
prism.publicationNameFrontiers in Immunology
prism.volume9
dc.identifier.doi10.17863/CAM.30858
dcterms.dateAccepted2018-05-28
rioxxterms.versionofrecord10.3389/fimmu.2018.01324
rioxxterms.versionVoR
rioxxterms.licenseref.urihttp://creativecommons.org/licenses/by/4.0/
rioxxterms.licenseref.startdate2018-05-28
dc.identifier.eissn1664-3224
rioxxterms.typeJournal Article/Review
pubs.funder-project-idWellcome Trust (106260/Z/14/Z)
pubs.funder-project-idEuropean Research Council (648889)
cam.issuedOnline2018-06-18
rioxxterms.freetoread.startdate2100-01-01


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Attribution 4.0 International
Except where otherwise noted, this item's licence is described as Attribution 4.0 International