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Article: Insulin-like growth factor I promotes cord blood T cell maturation through monocytes and inhibits their apoptosis in part through interleukin-6

TitleInsulin-like growth factor I promotes cord blood T cell maturation through monocytes and inhibits their apoptosis in part through interleukin-6
Authors
Issue Date2008
PublisherBioMed Central Ltd. The Journal's web site is located at http://www.biomedcentral.com/bmcimmunol/
Citation
Bmc Immunology, 2008, v. 9 How to Cite?
AbstractBackground: The functional immaturity of T cells contributes to the susceptibility of neonates to infections and the less severe graft-versus-host disease associated with cord blood (CB) transplantation. We have previously reported that insulin-like growth factor - I (IGF-I) promotes the phytohaemagglutinin (PHA)-induced CB T cell maturation and inhibits their apoptosis in mononuclear cell (MC) culture. We hypothesized that the effects of IGF-I may be mediated by accessory cells and soluble factors. Results: This study showed that the kinetics of PHA-induced maturation in purified CD3+ T cell was delayed compared to that in CBMC. The addition of autologous CD14+ monocytes increased T cell maturation and potentiated the effect of IGF-I. The addition of IL-6 had no effect on CB T cell maturation but it reduced PHA-induced apoptosis significantly. We further demonstrated that the neutralisation of IL-6 in CBMC culture partially abrogated the anti-apoptotic effect of IGF-1 on T cells. The anti-apoptotic effect of IL-6 was not mediated via the reduction of Fas expression in T cell subsets. Conclusion: Our results suggested that the maturation effect of IGF-1 is partially mediated by monocytes and the anti-apoptotic effect in part via IL-6. Further investigation is needed to explore the therapeutic use of IGF-I in enhancing neonatal immunity. © 2008 Law et al; licensee BioMed Central Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/125245
ISSN
2015 Impact Factor: 2.161
2015 SCImago Journal Rankings: 1.087
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
Research Grant Council of the Hong Kong Special Administrative Region, ChinaHKU7276/98M
Paediatrics Department Research FundPDRF12000-No5
Funding Information:

We thank the staff of the labour wards in Queen Mary Hospital and Tsan Yuk Hospital ( Hong Kong, SAR, China) in facilitating the collection of cord blood. The work described in this paper was partially supported by a grant from the Research Grant Council of the Hong Kong Special Administrative Region, China ( Project No. HKU7276/98M) and the Paediatrics Department Research Fund (PDRF12000-No5).

References

 

DC FieldValueLanguage
dc.contributor.authorLaw, HKWen_HK
dc.contributor.authorTu, Wen_HK
dc.contributor.authorLiu, Een_HK
dc.contributor.authorLau, YLen_HK
dc.date.accessioned2010-10-31T11:19:41Z-
dc.date.available2010-10-31T11:19:41Z-
dc.date.issued2008en_HK
dc.identifier.citationBmc Immunology, 2008, v. 9en_HK
dc.identifier.issn1471-2172en_HK
dc.identifier.urihttp://hdl.handle.net/10722/125245-
dc.description.abstractBackground: The functional immaturity of T cells contributes to the susceptibility of neonates to infections and the less severe graft-versus-host disease associated with cord blood (CB) transplantation. We have previously reported that insulin-like growth factor - I (IGF-I) promotes the phytohaemagglutinin (PHA)-induced CB T cell maturation and inhibits their apoptosis in mononuclear cell (MC) culture. We hypothesized that the effects of IGF-I may be mediated by accessory cells and soluble factors. Results: This study showed that the kinetics of PHA-induced maturation in purified CD3+ T cell was delayed compared to that in CBMC. The addition of autologous CD14+ monocytes increased T cell maturation and potentiated the effect of IGF-I. The addition of IL-6 had no effect on CB T cell maturation but it reduced PHA-induced apoptosis significantly. We further demonstrated that the neutralisation of IL-6 in CBMC culture partially abrogated the anti-apoptotic effect of IGF-1 on T cells. The anti-apoptotic effect of IL-6 was not mediated via the reduction of Fas expression in T cell subsets. Conclusion: Our results suggested that the maturation effect of IGF-1 is partially mediated by monocytes and the anti-apoptotic effect in part via IL-6. Further investigation is needed to explore the therapeutic use of IGF-I in enhancing neonatal immunity. © 2008 Law et al; licensee BioMed Central Ltd.en_HK
dc.languageengen_HK
dc.publisherBioMed Central Ltd. The Journal's web site is located at http://www.biomedcentral.com/bmcimmunol/en_HK
dc.relation.ispartofBMC Immunologyen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.rightsB M C Immunology. Copyright © BioMed Central Ltd.-
dc.subject.meshAntigens, CD45 - genetics - immunology - metabolism-
dc.subject.meshAntigens, CD95 - genetics - immunology - metabolism-
dc.subject.meshCell Differentiation - immunology-
dc.subject.meshInsulin-Like Growth Factor I - immunology - metabolism-
dc.subject.meshInterleukin-6 - immunology - metabolism-
dc.titleInsulin-like growth factor I promotes cord blood T cell maturation through monocytes and inhibits their apoptosis in part through interleukin-6en_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1471-2172&volume=9&issue=74&spage=&epage=&date=2008&atitle=Insulin-like+growth+factor+I+promotes+cord+blood+T+cell+maturation+through+monocytes+and+inhibits+their+apoptosis+in+part+through+interleukin-6en_HK
dc.identifier.emailTu, W:wwtu@hkucc.hku.hken_HK
dc.identifier.emailLau, YL:lauylung@hkucc.hku.hken_HK
dc.identifier.authorityTu, W=rp00416en_HK
dc.identifier.authorityLau, YL=rp00361en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1186/1471-2172-9-74en_HK
dc.identifier.pmid19091070-
dc.identifier.pmcidPMC2631546-
dc.identifier.scopuseid_2-s2.0-60649118952en_HK
dc.identifier.hkuros179390en_HK
dc.identifier.hkuros155949-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-60649118952&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume9en_HK
dc.identifier.issue74-
dc.identifier.isiWOS:000263235900001-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridLaw, HKW=7101939394en_HK
dc.identifier.scopusauthoridTu, W=7006479236en_HK
dc.identifier.scopusauthoridLiu, E=7202240063en_HK
dc.identifier.scopusauthoridLau, YL=7201403380en_HK
dc.identifier.citeulike3804045-

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