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Article: Notch ligation by Delta1 inhibits peripheral immune responses to transplantation antigens by a CD8 + cell-dependent mechanism

TitleNotch ligation by Delta1 inhibits peripheral immune responses to transplantation antigens by a CD8 + cell-dependent mechanism
Authors
Issue Date2003
PublisherAmerican Society for Clinical Investigation. The Journal's web site is located at http://www.jci.org
Citation
Journal Of Clinical Investigation, 2003, v. 112 n. 11, p. 1741-1750 How to Cite?
AbstractNotch signaling plays a fundamental role in determining the outcome of differentiation processes in many tissues. Notch signaling has been implicated in T versus B cell lineage commitment, thymic differentiation, and bone marrow hematopoietic precursor renewal and differentiation. Notch receptors and their ligands are also expressed on the surface of mature lymphocytes and APCs, but the effects of Notch signaling in the peripheral immune system remain poorly defined. The aim of the studies reported here was to investigate the effects of signaling through the Notch receptor using a ligand of the Delta-like family. We show that Notch ligation in the mature immune system markedly decreases responses to transplantation antigens. Constitutive expression of Delta-like 1 on alloantigen-bearing cells renders them nonimmunogenic and able to induce specific unresponsiveness to a challenge with the same alloantigen, even in the form of a cardiac allograft. These effects could be reversed by depletion of CD8 + cells at the time of transplantation. Ligation of Notch on splenic CD8 + cells results in a dramatic decrease in IFN-γ with a concomitant enhancement of IL-10 production, suggesting that Notch signaling can alter the differentiation potential of CD8 + cells. These data implicate Notch signaling in regulation of peripheral immunity and suggest a novel approach for manipulating deleterious immune responses.
Persistent Identifierhttp://hdl.handle.net/10722/172847
ISSN
2023 Impact Factor: 13.3
2023 SCImago Journal Rankings: 4.833
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWong, KKen_US
dc.contributor.authorCarpenter, MJen_US
dc.contributor.authorYoung, LLen_US
dc.contributor.authorWalker, SJen_US
dc.contributor.authorMckenzie, Gen_US
dc.contributor.authorRust, AJen_US
dc.contributor.authorWard, Gen_US
dc.contributor.authorPackwood, Len_US
dc.contributor.authorWahl, Ken_US
dc.contributor.authorDelriviere, Len_US
dc.contributor.authorHoyne, Gen_US
dc.contributor.authorGibbs, Pen_US
dc.contributor.authorChampion, BRen_US
dc.contributor.authorLamb, JRen_US
dc.contributor.authorDallman, MJen_US
dc.date.accessioned2012-10-30T06:25:19Z-
dc.date.available2012-10-30T06:25:19Z-
dc.date.issued2003en_US
dc.identifier.citationJournal Of Clinical Investigation, 2003, v. 112 n. 11, p. 1741-1750en_US
dc.identifier.issn0021-9738en_US
dc.identifier.urihttp://hdl.handle.net/10722/172847-
dc.description.abstractNotch signaling plays a fundamental role in determining the outcome of differentiation processes in many tissues. Notch signaling has been implicated in T versus B cell lineage commitment, thymic differentiation, and bone marrow hematopoietic precursor renewal and differentiation. Notch receptors and their ligands are also expressed on the surface of mature lymphocytes and APCs, but the effects of Notch signaling in the peripheral immune system remain poorly defined. The aim of the studies reported here was to investigate the effects of signaling through the Notch receptor using a ligand of the Delta-like family. We show that Notch ligation in the mature immune system markedly decreases responses to transplantation antigens. Constitutive expression of Delta-like 1 on alloantigen-bearing cells renders them nonimmunogenic and able to induce specific unresponsiveness to a challenge with the same alloantigen, even in the form of a cardiac allograft. These effects could be reversed by depletion of CD8 + cells at the time of transplantation. Ligation of Notch on splenic CD8 + cells results in a dramatic decrease in IFN-γ with a concomitant enhancement of IL-10 production, suggesting that Notch signaling can alter the differentiation potential of CD8 + cells. These data implicate Notch signaling in regulation of peripheral immunity and suggest a novel approach for manipulating deleterious immune responses.en_US
dc.languageengen_US
dc.publisherAmerican Society for Clinical Investigation. The Journal's web site is located at http://www.jci.orgen_US
dc.relation.ispartofJournal of Clinical Investigationen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAntigen-Presenting Cells - Physiologyen_US
dc.subject.meshApoptosisen_US
dc.subject.meshCd8-Positive T-Lymphocytes - Immunologyen_US
dc.subject.meshCho Cellsen_US
dc.subject.meshCalcium-Binding Proteinsen_US
dc.subject.meshCricetinaeen_US
dc.subject.meshGraft Rejection - Prevention & Controlen_US
dc.subject.meshHistocompatibility Antigens - Immunologyen_US
dc.subject.meshIntercellular Signaling Peptides And Proteinsen_US
dc.subject.meshInterferon-Gamma - Biosynthesisen_US
dc.subject.meshInterleukin-10 - Biosynthesisen_US
dc.subject.meshIntracellular Signaling Peptides And Proteinsen_US
dc.subject.meshMembrane Proteins - Physiologyen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Inbred Strainsen_US
dc.subject.meshProteins - Physiologyen_US
dc.subject.meshReceptor, Notch2en_US
dc.subject.meshReceptors, Cell Surface - Physiologyen_US
dc.subject.meshSignal Transduction - Physiologyen_US
dc.subject.meshTransfectionen_US
dc.titleNotch ligation by Delta1 inhibits peripheral immune responses to transplantation antigens by a CD8 + cell-dependent mechanismen_US
dc.typeArticleen_US
dc.identifier.emailWong, KK: kkywong@hkucc.hku.hken_US
dc.identifier.authorityWong, KK=rp01392en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1172/JCI200318020en_US
dc.identifier.pmid14660750-
dc.identifier.scopuseid_2-s2.0-0347951391en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0347951391&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume112en_US
dc.identifier.issue11en_US
dc.identifier.spage1741en_US
dc.identifier.epage1750en_US
dc.identifier.isiWOS:000187111800019-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridWong, KK=24438686400en_US
dc.identifier.scopusauthoridCarpenter, MJ=7201447672en_US
dc.identifier.scopusauthoridYoung, LL=7403664904en_US
dc.identifier.scopusauthoridWalker, SJ=7403745290en_US
dc.identifier.scopusauthoridMcKenzie, G=7004966341en_US
dc.identifier.scopusauthoridRust, AJ=7003933935en_US
dc.identifier.scopusauthoridWard, G=8364574300en_US
dc.identifier.scopusauthoridPackwood, L=6507619103en_US
dc.identifier.scopusauthoridWahl, K=8251690400en_US
dc.identifier.scopusauthoridDelriviere, L=6701765051en_US
dc.identifier.scopusauthoridHoyne, G=6701845755en_US
dc.identifier.scopusauthoridGibbs, P=7103114776en_US
dc.identifier.scopusauthoridChampion, BR=7003728991en_US
dc.identifier.scopusauthoridLamb, JR=7201524642en_US
dc.identifier.scopusauthoridDallman, MJ=35473592200en_US
dc.identifier.issnl0021-9738-

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