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Article: Novel immunomodulatory effects of adiponectin on dendritic cell functions

TitleNovel immunomodulatory effects of adiponectin on dendritic cell functions
Authors
KeywordsAdiponectin
Dendritic cell
Immunomodulation
Programmed death-1 ligand
Issue Date2011
PublisherElsevier Ltd. The Journal's web site is located at http://www.elsevier.com/locate/intimp
Citation
International Immunopharmacology, 2011, v. 11 n. 5, p. 604-609 How to Cite?
Abstract
Adiponectin (ADN) is an adipocytokine with anti-inflammatory properties. Although it has been reported that ADN can inhibit the immunostimulatory function of monocytes and macrophages, little is known of its effect on dendritic cells (DC). Recent data suggest that ADN can regulate immune responses. DCs are uniquely specialised antigen presenting cells that play a central role in the initiation of immunity and tolerance. In this study, we have investigated the immuno- modulatory effects of ADN on DC functions. We found that ADN has only moderate effect on the differentiation of murine bone marrow (BM) derived DCs but altered the phenotype of DCs. The expression of major histocompatibilty complex class II (MHCII), CD80 and CD86 on ADN conditioned DCs (ADN-DCs) was lower than that on untreated cells. The production of IL-12p40 was also suppressed in ADN-DCs. Interestingly, ADN treated DCs showed an increase in the expression of the inhibitory molecule, programmed death-1 ligand (PDL-1) compared to untreated cells. In vitro co-culture of ADN-DCs with allogeneic T cells led to a decrease in T cell proliferation and reduction of IL-2 production. Concomitant with that, a higher percentage of CD4 +CD25 +Foxp3 + regulatory T cells (Tregs) was detected in co-cultures of T cells and ADN-DCs. Blocking PD-1/PDL-1 pathway could partially restore T cell function. These findings suggest that the immunomodulatory effect of ADN on immune responses could be at least partially be mediated by its ability to alter DC function. The PD-1/PDL-1 pathway and the enhancement of Treg expansion are implicated in the immunomodulatory mechanisms. © 2010 Elsevier B.V.
Persistent Identifierhttp://hdl.handle.net/10722/133655
ISSN
2013 Impact Factor: 2.711
2013 SCImago Journal Rankings: 0.970
ISI Accession Number ID
Funding AgencyGrant Number
HKU762108M
Funding Information:

This work is supported by research grant from the Hong Kong General Research Fund (HKU 762108M).

References

 

Author Affiliations
  1. The University of Hong Kong
  2. Imperial College London
DC FieldValueLanguage
dc.contributor.authorTsang, JYSen_HK
dc.contributor.authorLi, Den_HK
dc.contributor.authorHo, Den_HK
dc.contributor.authorPeng, Jen_HK
dc.contributor.authorXu, Aen_HK
dc.contributor.authorLamb, Jen_HK
dc.contributor.authorChen, Yen_HK
dc.contributor.authorTam, PKHen_HK
dc.date.accessioned2011-05-24T02:13:40Z-
dc.date.available2011-05-24T02:13:40Z-
dc.date.issued2011en_HK
dc.identifier.citationInternational Immunopharmacology, 2011, v. 11 n. 5, p. 604-609en_HK
dc.identifier.issn1567-5769en_HK
dc.identifier.urihttp://hdl.handle.net/10722/133655-
dc.description.abstractAdiponectin (ADN) is an adipocytokine with anti-inflammatory properties. Although it has been reported that ADN can inhibit the immunostimulatory function of monocytes and macrophages, little is known of its effect on dendritic cells (DC). Recent data suggest that ADN can regulate immune responses. DCs are uniquely specialised antigen presenting cells that play a central role in the initiation of immunity and tolerance. In this study, we have investigated the immuno- modulatory effects of ADN on DC functions. We found that ADN has only moderate effect on the differentiation of murine bone marrow (BM) derived DCs but altered the phenotype of DCs. The expression of major histocompatibilty complex class II (MHCII), CD80 and CD86 on ADN conditioned DCs (ADN-DCs) was lower than that on untreated cells. The production of IL-12p40 was also suppressed in ADN-DCs. Interestingly, ADN treated DCs showed an increase in the expression of the inhibitory molecule, programmed death-1 ligand (PDL-1) compared to untreated cells. In vitro co-culture of ADN-DCs with allogeneic T cells led to a decrease in T cell proliferation and reduction of IL-2 production. Concomitant with that, a higher percentage of CD4 +CD25 +Foxp3 + regulatory T cells (Tregs) was detected in co-cultures of T cells and ADN-DCs. Blocking PD-1/PDL-1 pathway could partially restore T cell function. These findings suggest that the immunomodulatory effect of ADN on immune responses could be at least partially be mediated by its ability to alter DC function. The PD-1/PDL-1 pathway and the enhancement of Treg expansion are implicated in the immunomodulatory mechanisms. © 2010 Elsevier B.V.en_HK
dc.languageengen_US
dc.publisherElsevier Ltd. The Journal's web site is located at http://www.elsevier.com/locate/intimpen_HK
dc.relation.ispartofInternational Immunopharmacologyen_HK
dc.subjectAdiponectinen_HK
dc.subjectDendritic cellen_HK
dc.subjectImmunomodulationen_HK
dc.subjectProgrammed death-1 liganden_HK
dc.titleNovel immunomodulatory effects of adiponectin on dendritic cell functionsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1567-5769&volume=11&issue=5&spage=604&epage=609&date=2011&atitle=Novel+immunomodulatory+effects+of+adiponectin+on+dendritic+cell+functions-
dc.identifier.emailXu, A:amxu@hkucc.hku.hken_HK
dc.identifier.emailChen, Y:ychenc@hkucc.hku.hken_HK
dc.identifier.emailTam, PKH:paultam@hkucc.hku.hken_HK
dc.identifier.authorityXu, A=rp00485en_HK
dc.identifier.authorityChen, Y=rp01318en_HK
dc.identifier.authorityTam, PKH=rp00060en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.intimp.2010.11.009en_HK
dc.identifier.pmid21094289en_HK
dc.identifier.scopuseid_2-s2.0-79954631240en_HK
dc.identifier.hkuros185390en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-79954631240&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume11en_HK
dc.identifier.issue5en_HK
dc.identifier.spage604en_HK
dc.identifier.epage609en_HK
dc.identifier.isiWOS:000291069700012-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridTsang, JYS=15081781300en_HK
dc.identifier.scopusauthoridLi, D=53264079000en_HK
dc.identifier.scopusauthoridHo, D=53263908500en_HK
dc.identifier.scopusauthoridPeng, J=49961959700en_HK
dc.identifier.scopusauthoridXu, A=7202655409en_HK
dc.identifier.scopusauthoridLamb, J=7201524642en_HK
dc.identifier.scopusauthoridChen, Y=36463185300en_HK
dc.identifier.scopusauthoridTam, PKH=7202539421en_HK
dc.identifier.citeulike8366256-

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