File Download
 
Links for fulltext
(May Require Subscription)
 
Supplementary

Article: Phenotypic and functional abnormalities of bone marrow-derived dendritic cells in systemic lupus erythematosus
  • Basic View
  • Metadata View
  • XML View
TitlePhenotypic and functional abnormalities of bone marrow-derived dendritic cells in systemic lupus erythematosus
 
AuthorsNie, YJ1
Mok, MY1
Chan, GCF1
Chan, AW1
Jin, O1
Kavikondala, S1
Lie, AKW1
Lau, CS1
 
Issue Date2010
 
PublisherBioMed Central Ltd. The Journal's web site is located at http://arthritis-research.com/
 
CitationArthritis Research And Therapy, 2010, v. 12 n. 3 [How to Cite?]
DOI: http://dx.doi.org/10.1186/ar3018
 
AbstractIntroduction: Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by autoreactive T and B cells, which are believed to be secondary to deficient dendritic cells (DCs). However, whether DC abnormalities occur during their development in the bone marrow (BM) or in the periphery is not known.Methods: Thirteen patients with SLE and 16 normal controls were recruited. We studied the morphology, phenotype, and functional abilities of bone marrow-derived dendritic cells (BMDCs) generated by using two culture methods: FMS-like tyrosine kinase 3 (Flt3)-ligand (FL) and granulocyte-macrophage colony-stimulating factor (GM-CSF) plus interleukin-4 (IL-4), respectively.Results: BMDCs induced by FL exhibited both myeloid (mDC) and plasmacytoid DC (pDC) features, whereas GM-CSF/IL-4 induced mDC generation. Substantial phenotypic and functional defects of BMDCs were found from patients with SLE at different stages of cell maturation. When compared with healthy controls, SLE immature BM FLDCs expressed higher levels of CCR7. Both immature and mature SLE BM FLDCs expressed higher levels of CD40 and CD86 and induced stronger T-cell proliferation. SLE BM mDCs expressed higher levels of CD40 and CD86 but lower levels of HLA-DR and a lower ability to stimulate T-cell proliferation when compared with control BM mDCs.Conclusions: Our data are in accordance with previous reports that suggest that DCs have a potential pathogenic role in SLE. Defects of these cells are evident during their development in BM. BM mDCs are deficient, whereas BM pDCs, which are part of BM FLDCs, are the likely culprit in inducing autoimmunity in SLE. © 2010 Nie et al.; licensee BioMed Central Ltd.
 
ISSN1478-6354
2012 Impact Factor: 4.302
2012 SCImago Journal Rankings: 1.814
 
DOIhttp://dx.doi.org/10.1186/ar3018
 
PubMed Central IDPMC2911875
 
ISI Accession Number IDWOS:000280227900036
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorNie, YJ
 
dc.contributor.authorMok, MY
 
dc.contributor.authorChan, GCF
 
dc.contributor.authorChan, AW
 
dc.contributor.authorJin, O
 
dc.contributor.authorKavikondala, S
 
dc.contributor.authorLie, AKW
 
dc.contributor.authorLau, CS
 
dc.date.accessioned2010-10-31T11:06:11Z
 
dc.date.available2010-10-31T11:06:11Z
 
dc.date.issued2010
 
dc.description.abstractIntroduction: Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by autoreactive T and B cells, which are believed to be secondary to deficient dendritic cells (DCs). However, whether DC abnormalities occur during their development in the bone marrow (BM) or in the periphery is not known.Methods: Thirteen patients with SLE and 16 normal controls were recruited. We studied the morphology, phenotype, and functional abilities of bone marrow-derived dendritic cells (BMDCs) generated by using two culture methods: FMS-like tyrosine kinase 3 (Flt3)-ligand (FL) and granulocyte-macrophage colony-stimulating factor (GM-CSF) plus interleukin-4 (IL-4), respectively.Results: BMDCs induced by FL exhibited both myeloid (mDC) and plasmacytoid DC (pDC) features, whereas GM-CSF/IL-4 induced mDC generation. Substantial phenotypic and functional defects of BMDCs were found from patients with SLE at different stages of cell maturation. When compared with healthy controls, SLE immature BM FLDCs expressed higher levels of CCR7. Both immature and mature SLE BM FLDCs expressed higher levels of CD40 and CD86 and induced stronger T-cell proliferation. SLE BM mDCs expressed higher levels of CD40 and CD86 but lower levels of HLA-DR and a lower ability to stimulate T-cell proliferation when compared with control BM mDCs.Conclusions: Our data are in accordance with previous reports that suggest that DCs have a potential pathogenic role in SLE. Defects of these cells are evident during their development in BM. BM mDCs are deficient, whereas BM pDCs, which are part of BM FLDCs, are the likely culprit in inducing autoimmunity in SLE. © 2010 Nie et al.; licensee BioMed Central Ltd.
 
dc.description.naturepublished_or_final_version
 
dc.identifier.citationArthritis Research And Therapy, 2010, v. 12 n. 3 [How to Cite?]
DOI: http://dx.doi.org/10.1186/ar3018
 
dc.identifier.doihttp://dx.doi.org/10.1186/ar3018
 
dc.identifier.eissn1478-6362
 
dc.identifier.hkuros174737
 
dc.identifier.hkuros195367
 
dc.identifier.hkuros206497
 
dc.identifier.hkuros163822
 
dc.identifier.isiWOS:000280227900036
 
dc.identifier.issn1478-6354
2012 Impact Factor: 4.302
2012 SCImago Journal Rankings: 1.814
 
dc.identifier.issue3
 
dc.identifier.openurl
 
dc.identifier.pmcidPMC2911875
 
dc.identifier.pmid20478074
 
dc.identifier.scopuseid_2-s2.0-77952255629
 
dc.identifier.spageR91
 
dc.identifier.urihttp://hdl.handle.net/10722/125005
 
dc.identifier.volume12
 
dc.languageeng
 
dc.publisherBioMed Central Ltd. The Journal's web site is located at http://arthritis-research.com/
 
dc.publisher.placeUnited Kingdom
 
dc.relation.ispartofArthritis Research and Therapy
 
dc.relation.referencesReferences in Scopus
 
dc.rightsArthritis Research & Therapy. Copyright © BioMed Central Ltd.
 
dc.subject.meshAdult
 
dc.subject.meshBone Marrow Cells - pathology
 
dc.subject.meshDendritic Cells - drug effects - pathology - physiology
 
dc.subject.meshLupus Erythematosus, Systemic - pathology - physiopathology
 
dc.subject.meshPhenotype
 
dc.titlePhenotypic and functional abnormalities of bone marrow-derived dendritic cells in systemic lupus erythematosus
 
dc.typeArticle
 
<?xml encoding="utf-8" version="1.0"?>
<item><contributor.author>Nie, YJ</contributor.author>
<contributor.author>Mok, MY</contributor.author>
<contributor.author>Chan, GCF</contributor.author>
<contributor.author>Chan, AW</contributor.author>
<contributor.author>Jin, O</contributor.author>
<contributor.author>Kavikondala, S</contributor.author>
<contributor.author>Lie, AKW</contributor.author>
<contributor.author>Lau, CS</contributor.author>
<date.accessioned>2010-10-31T11:06:11Z</date.accessioned>
<date.available>2010-10-31T11:06:11Z</date.available>
<date.issued>2010</date.issued>
<identifier.citation>Arthritis Research And Therapy, 2010, v. 12 n. 3</identifier.citation>
<identifier.issn>1478-6354</identifier.issn>
<identifier.uri>http://hdl.handle.net/10722/125005</identifier.uri>
<description.abstract>Introduction: Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by autoreactive T and B cells, which are believed to be secondary to deficient dendritic cells (DCs). However, whether DC abnormalities occur during their development in the bone marrow (BM) or in the periphery is not known.Methods: Thirteen patients with SLE and 16 normal controls were recruited. We studied the morphology, phenotype, and functional abilities of bone marrow-derived dendritic cells (BMDCs) generated by using two culture methods: FMS-like tyrosine kinase 3 (Flt3)-ligand (FL) and granulocyte-macrophage colony-stimulating factor (GM-CSF) plus interleukin-4 (IL-4), respectively.Results: BMDCs induced by FL exhibited both myeloid (mDC) and plasmacytoid DC (pDC) features, whereas GM-CSF/IL-4 induced mDC generation. Substantial phenotypic and functional defects of BMDCs were found from patients with SLE at different stages of cell maturation. When compared with healthy controls, SLE immature BM FLDCs expressed higher levels of CCR7. Both immature and mature SLE BM FLDCs expressed higher levels of CD40 and CD86 and induced stronger T-cell proliferation. SLE BM mDCs expressed higher levels of CD40 and CD86 but lower levels of HLA-DR and a lower ability to stimulate T-cell proliferation when compared with control BM mDCs.Conclusions: Our data are in accordance with previous reports that suggest that DCs have a potential pathogenic role in SLE. Defects of these cells are evident during their development in BM. BM mDCs are deficient, whereas BM pDCs, which are part of BM FLDCs, are the likely culprit in inducing autoimmunity in SLE. &#169; 2010 Nie et al.; licensee BioMed Central Ltd.</description.abstract>
<language>eng</language>
<publisher>BioMed Central Ltd. The Journal&apos;s web site is located at http://arthritis-research.com/</publisher>
<relation.ispartof>Arthritis Research and Therapy</relation.ispartof>
<rights>Arthritis Research &amp; Therapy. Copyright &#169; BioMed Central Ltd.</rights>
<subject.mesh>Adult</subject.mesh>
<subject.mesh>Bone Marrow Cells - pathology</subject.mesh>
<subject.mesh>Dendritic Cells - drug effects - pathology - physiology</subject.mesh>
<subject.mesh>Lupus Erythematosus, Systemic - pathology - physiopathology</subject.mesh>
<subject.mesh>Phenotype</subject.mesh>
<title>Phenotypic and functional abnormalities of bone marrow-derived dendritic cells in systemic lupus erythematosus</title>
<type>Article</type>
<identifier.openurl>http://library.hku.hk:4550/resserv?sid=HKU:IR&amp;issn=1478-6354&amp;volume=12&amp;issue=3&amp;spage=R91&amp;epage=&amp;date=2010&amp;atitle=Phenotypic+and+functional+abnormalities+of+bone+marrow-derived+dendritic+cells+in+systemic+lupus+erythematosus</identifier.openurl>
<description.nature>published_or_final_version</description.nature>
<identifier.doi>10.1186/ar3018</identifier.doi>
<identifier.pmid>20478074</identifier.pmid>
<identifier.pmcid>PMC2911875</identifier.pmcid>
<identifier.scopus>eid_2-s2.0-77952255629</identifier.scopus>
<identifier.hkuros>174737</identifier.hkuros>
<identifier.hkuros>195367</identifier.hkuros>
<identifier.hkuros>206497</identifier.hkuros>
<identifier.hkuros>163822</identifier.hkuros>
<relation.references>http://www.scopus.com/mlt/select.url?eid=2-s2.0-77952255629&amp;selection=ref&amp;src=s&amp;origin=recordpage</relation.references>
<identifier.volume>12</identifier.volume>
<identifier.issue>3</identifier.issue>
<identifier.spage>R91</identifier.spage>
<identifier.eissn>1478-6362</identifier.eissn>
<identifier.isi>WOS:000280227900036</identifier.isi>
<publisher.place>United Kingdom</publisher.place>
<bitstream.url>http://hub.hku.hk/bitstream/10722/125005/1/ar3018.pdf</bitstream.url>
</item>
Author Affiliations
  1. The University of Hong Kong Li Ka Shing Faculty of Medicine