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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
Title | Insulin-like growth factor 1 promotes cord blood T cell maturation and inhibits its spontaneous and phytohemagglutinin-induced apoptosis through different mechanisms |
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Authors | |
Issue Date | 2000 |
Publisher | American 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? |
Abstract | Functional 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 Identifier | http://hdl.handle.net/10722/49268 |
ISSN | 2021 Impact Factor: 5.426 2020 SCImago Journal Rankings: 2.737 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
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dc.contributor.author | Tu, W | en_HK |
dc.contributor.author | Cheung, PT | en_HK |
dc.contributor.author | Lau, YL | en_HK |
dc.date.accessioned | 2008-06-12T06:38:04Z | - |
dc.date.available | 2008-06-12T06:38:04Z | - |
dc.date.issued | 2000 | en_HK |
dc.identifier.citation | Journal Of Immunology, 2000, v. 165 n. 3, p. 1331-1336 | en_HK |
dc.identifier.issn | 0022-1767 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/49268 | - |
dc.description.abstract | Functional 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.extent | 420 bytes | - |
dc.format.mimetype | text/html | - |
dc.language | eng | en_HK |
dc.publisher | American Association of Immunologists. The Journal's web site is located at http://www.jimmunol.org | en_HK |
dc.relation.ispartof | Journal of Immunology | en_HK |
dc.rights | This 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.org | en_HK |
dc.subject.mesh | Apoptosis - immunology | en_HK |
dc.subject.mesh | Fetal Blood - cytology - immunology - metabolism | en_HK |
dc.subject.mesh | Insulin-Like Growth Factor I - physiology | en_HK |
dc.subject.mesh | Phytohemagglutinins - antagonists & inhibitors - pharmacology | en_HK |
dc.subject.mesh | T-Lymphocytes - cytology - immunology - metabolism - physiology | en_HK |
dc.title | Insulin-like growth factor 1 promotes cord blood T cell maturation and inhibits its spontaneous and phytohemagglutinin-induced apoptosis through different mechanisms | en_HK |
dc.type | Article | en_HK |
dc.identifier.openurl | http://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+mechanisms | en_HK |
dc.identifier.email | Tu, W:wwtu@hkucc.hku.hk | en_HK |
dc.identifier.email | Cheung, PT:ptcheung@hkucc.hku.hk | en_HK |
dc.identifier.email | Lau, YL:lauylung@hkucc.hku.hk | en_HK |
dc.identifier.authority | Tu, W=rp00416 | en_HK |
dc.identifier.authority | Cheung, PT=rp00351 | en_HK |
dc.identifier.authority | Lau, YL=rp00361 | en_HK |
dc.description.nature | published_or_final_version | en_HK |
dc.identifier.doi | 10.4049/jimmunol.165.3.1331 | - |
dc.identifier.pmid | 10903734 | - |
dc.identifier.scopus | eid_2-s2.0-0034254438 | en_HK |
dc.identifier.hkuros | 49677 | - |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-0034254438&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 165 | en_HK |
dc.identifier.issue | 3 | en_HK |
dc.identifier.spage | 1331 | en_HK |
dc.identifier.epage | 1336 | en_HK |
dc.identifier.isi | WOS:000088340600022 | - |
dc.publisher.place | United States | en_HK |
dc.identifier.scopusauthorid | Tu, W=7006479236 | en_HK |
dc.identifier.scopusauthorid | Cheung, PT=7202595465 | en_HK |
dc.identifier.scopusauthorid | Lau, YL=7201403380 | en_HK |
dc.identifier.issnl | 0022-1767 | - |