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Article: Phenotypic and functional abnormalities of bone marrow-derived dendritic cells in systemic lupus erythematosus

TitlePhenotypic and functional abnormalities of bone marrow-derived dendritic cells in systemic lupus erythematosus
Authors
Issue Date2010
PublisherBioMed Central Ltd. The Journal's web site is located at http://arthritis-research.com/
Citation
Arthritis Research And Therapy, 2010, v. 12 n. 3 How to Cite?
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. © 2010 Nie et al.; licensee BioMed Central Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/125005
ISSN
2013 Impact Factor: 4.117
2013 SCImago Journal Rankings: 2.194
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorNie, YJen_HK
dc.contributor.authorMok, MYen_HK
dc.contributor.authorChan, GCFen_HK
dc.contributor.authorChan, AWen_HK
dc.contributor.authorJin, Oen_HK
dc.contributor.authorKavikondala, Sen_HK
dc.contributor.authorLie, AKWen_HK
dc.contributor.authorLau, CSen_HK
dc.date.accessioned2010-10-31T11:06:11Z-
dc.date.available2010-10-31T11:06:11Z-
dc.date.issued2010en_HK
dc.identifier.citationArthritis Research And Therapy, 2010, v. 12 n. 3en_HK
dc.identifier.issn1478-6354en_HK
dc.identifier.urihttp://hdl.handle.net/10722/125005-
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.en_HK
dc.languageengen_HK
dc.publisherBioMed Central Ltd. The Journal's web site is located at http://arthritis-research.com/en_HK
dc.relation.ispartofArthritis Research and Therapyen_HK
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 erythematosusen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1478-6354&volume=12&issue=3&spage=R91&epage=&date=2010&atitle=Phenotypic+and+functional+abnormalities+of+bone+marrow-derived+dendritic+cells+in+systemic+lupus+erythematosus-
dc.identifier.emailMok, MY:temy@hkucc.hku.hken_HK
dc.identifier.emailChan, GCF:gcfchan@hkucc.hku.hken_HK
dc.identifier.emailLau, CS:cslau@hku.hken_HK
dc.identifier.authorityMok, MY=rp00490en_HK
dc.identifier.authorityChan, GCF=rp00431en_HK
dc.identifier.authorityLau, CS=rp01348en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1186/ar3018en_HK
dc.identifier.pmid20478074-
dc.identifier.pmcidPMC2911875-
dc.identifier.scopuseid_2-s2.0-77952255629en_HK
dc.identifier.hkuros174737en_HK
dc.identifier.hkuros195367en_US
dc.identifier.hkuros206497-
dc.identifier.hkuros163822-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77952255629&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume12en_HK
dc.identifier.issue3en_HK
dc.identifier.spageR91en_HK
dc.identifier.eissn1478-6362-
dc.identifier.isiWOS:000280227900036-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridNie, YJ=15072918200en_HK
dc.identifier.scopusauthoridMok, MY=7006024184en_HK
dc.identifier.scopusauthoridChan, GCF=16160154400en_HK
dc.identifier.scopusauthoridChan, AW=7403168355en_HK
dc.identifier.scopusauthoridJin, O=7004432895en_HK
dc.identifier.scopusauthoridKavikondala, S=14819602600en_HK
dc.identifier.scopusauthoridLie, AKW=7004510870en_HK
dc.identifier.scopusauthoridLau, CS=14035682100en_HK

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