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Article: Insulin-like growth factor 1 promotes cord blood T cell maturation and inhibits its spontaneous and phytohemagglutinin-induced apoptosis through different mechanisms

TitleInsulin-like growth factor 1 promotes cord blood T cell maturation and inhibits its spontaneous and phytohemagglutinin-induced apoptosis through different mechanisms
Authors
Issue Date2000
PublisherAmerican Association of Immunologists. The Journal's web site is located at http://www.jimmunol.org
Citation
Journal Of Immunology, 2000, v. 165 n. 3, p. 1331-1336 How to Cite?
AbstractFunctional immaturity of neonatal T cells is related to their immature phenotype, with the majority of neonatal T cells of naive (CD45RA+T cells. The progression of T cells from naive cells to effector cells is dependent on the survival of Ag-specific T cells and their resistance to apoptosis. In this study, we showed for the first time that insulin-like growth factor 1 (IGF-1) converted cord blood CD45RA+ T cells to CD45RO+ T cells and inhibited cord blood T cell apoptosis. We found cord blood T cells stimulated with PHA would result in gradual loss of CD45RA and gain of CD45RO expression. IGF-1 further increased the loss of CD45RA and enhanced CD45RO expression in PHA-stimulated cord blood T cells. In addition, IGF-1 prevented cord blood T cells from spontaneous apoptosis through a mechanism other than Fas/FasL. In PHA-activated cord blood T cells, IGF-1 prevented both naive (CD45RA+) and memory/mature (CD45RO+) T cells from apoptosis. Moreover, cord blood T cells cultured with IGF-1 and PHA had a higher resistance to anti-Fas-induced apoptosis as compared with PHA-activated cord blood T cells. IGF-1 also significantly inhibited PHA-induced Fas expression on cord blood T cells. These results demonstrate that IGF-1 promotes the maturation and maintains the survival of cord blood T cells. Its antiapoptotic effect in PHA-activated cord blood T cells may be mediated through the down-regulation of Fas expression.
Persistent Identifierhttp://hdl.handle.net/10722/49268
ISSN
2015 Impact Factor: 4.985
2015 SCImago Journal Rankings: 3.549
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorTu, Wen_HK
dc.contributor.authorCheung, PTen_HK
dc.contributor.authorLau, YLen_HK
dc.date.accessioned2008-06-12T06:38:04Z-
dc.date.available2008-06-12T06:38:04Z-
dc.date.issued2000en_HK
dc.identifier.citationJournal Of Immunology, 2000, v. 165 n. 3, p. 1331-1336en_HK
dc.identifier.issn0022-1767en_HK
dc.identifier.urihttp://hdl.handle.net/10722/49268-
dc.description.abstractFunctional immaturity of neonatal T cells is related to their immature phenotype, with the majority of neonatal T cells of naive (CD45RA+T cells. The progression of T cells from naive cells to effector cells is dependent on the survival of Ag-specific T cells and their resistance to apoptosis. In this study, we showed for the first time that insulin-like growth factor 1 (IGF-1) converted cord blood CD45RA+ T cells to CD45RO+ T cells and inhibited cord blood T cell apoptosis. We found cord blood T cells stimulated with PHA would result in gradual loss of CD45RA and gain of CD45RO expression. IGF-1 further increased the loss of CD45RA and enhanced CD45RO expression in PHA-stimulated cord blood T cells. In addition, IGF-1 prevented cord blood T cells from spontaneous apoptosis through a mechanism other than Fas/FasL. In PHA-activated cord blood T cells, IGF-1 prevented both naive (CD45RA+) and memory/mature (CD45RO+) T cells from apoptosis. Moreover, cord blood T cells cultured with IGF-1 and PHA had a higher resistance to anti-Fas-induced apoptosis as compared with PHA-activated cord blood T cells. IGF-1 also significantly inhibited PHA-induced Fas expression on cord blood T cells. These results demonstrate that IGF-1 promotes the maturation and maintains the survival of cord blood T cells. Its antiapoptotic effect in PHA-activated cord blood T cells may be mediated through the down-regulation of Fas expression.en_HK
dc.format.extent420 bytes-
dc.format.mimetypetext/html-
dc.languageengen_HK
dc.publisherAmerican Association of Immunologists. The Journal's web site is located at http://www.jimmunol.orgen_HK
dc.relation.ispartofJournal of Immunologyen_HK
dc.rightsThis is an author-produced version of a manuscript accepted for publication in The Journal of Immunology (The JI). The American Association of Immunologists, Inc. (The AAI), publisher of The JI, holds the copyright to this manuscript. This manuscript has not yet been copyedited or subjected to editorial proofreading by The JI; hence, it may differ from the final version published in The JI (online and in print). The AAI (The JI) is not liable for errors or omissions in this author-produced version of the manuscript or in any version derived from it by the National Institutes of Health or any other third party. The final, citable version of record can be found at www.jimmunol.orgen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subject.meshApoptosis - immunologyen_HK
dc.subject.meshFetal Blood - cytology - immunology - metabolismen_HK
dc.subject.meshInsulin-Like Growth Factor I - physiologyen_HK
dc.subject.meshPhytohemagglutinins - antagonists & inhibitors - pharmacologyen_HK
dc.subject.meshT-Lymphocytes - cytology - immunology - metabolism - physiologyen_HK
dc.titleInsulin-like growth factor 1 promotes cord blood T cell maturation and inhibits its spontaneous and phytohemagglutinin-induced apoptosis through different mechanismsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-1767&volume=165&issue=3&spage=1331&epage=1336&date=2000&atitle=Insulin-like+growth+factor+1+promotes+cord+blood+T+cell+maturation+and+inhibits+its+spontaneous+and+phytohemagglutinin-induced+apoptosis+through+different+mechanismsen_HK
dc.identifier.emailTu, W:wwtu@hkucc.hku.hken_HK
dc.identifier.emailCheung, PT:ptcheung@hkucc.hku.hken_HK
dc.identifier.emailLau, YL:lauylung@hkucc.hku.hken_HK
dc.identifier.authorityTu, W=rp00416en_HK
dc.identifier.authorityCheung, PT=rp00351en_HK
dc.identifier.authorityLau, YL=rp00361en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.pmid10903734-
dc.identifier.scopuseid_2-s2.0-0034254438en_HK
dc.identifier.hkuros49677-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0034254438&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume165en_HK
dc.identifier.issue3en_HK
dc.identifier.spage1331en_HK
dc.identifier.epage1336en_HK
dc.identifier.isiWOS:000088340600022-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridTu, W=7006479236en_HK
dc.identifier.scopusauthoridCheung, PT=7202595465en_HK
dc.identifier.scopusauthoridLau, YL=7201403380en_HK

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