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Article: Abnormalities in circulating plasmacytoid dendritic cells in patients with systemic lupus erythematosus

TitleAbnormalities in circulating plasmacytoid dendritic cells in patients with 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. 4 How to Cite?
Abstract
Introduction: Dendritic cells (DCs) are capable of inducing immunity or tolerance. Previous studies have suggested plasmacytoid DCs (pDCs) are pathogenic in systemic lupus erythematosus (SLE). However, the functional characteristics of directly isolated peripheral circulating blood pDCs in SLE have not been evaluated previously.Methods: Peripheral blood pDCs from 62 healthy subjects and 58 SLE patients were treated with apoptotic cells derived from polymorphonuclear cells (PMNs). Antigen loaded or unloaded pDCs were then co-cultured with autologous or allogenous T cells. Changes in T cell proliferation, cell surface CD25 expression, intracellular Foxp3 expression and cytokine production were evaluated. pDCs that had captured apoptotic PMNs (pDCs + apoPMNs were also studied for their cytokine production (interferon (IFN)-alpha, interleukin (IL)-6, IL-10, IL-18) and toll like receptor (TLR) expression.Results: Circulating pDCs from SLE patients had an increased ability to stimulate T cells when compared with control pDCs. Using allogenous T cells as responder cells, SLE pDCs induced T cell proliferation even in the absence of apoptotic PMNs. In addition, healthy pDCs + apoPMNs induced suppressive T regulatory cell features with increased Foxp3 expression in CD4 + CD25 + cells while SLE pDCs + apoPMNs did not. There were differences in the cytokine profile of pDCs that had captured apoptotic PMNs between healthy subjects and patients with SLE. Healthy pDCs + apoPMNs showed decreased production of IL-6 but no significant changes in IL-10 and IL-18. These pDCs + apoPMNs also showed increased mRNA transcription of TLR9. On the other hand, while SLE pDCs + apoPMNs also had decreased IL-6, there was decreased IL-18 mRNA expression and persistent IL-10 protein synthesis. In addition, SLE pDCs lacked TLR9 recruitment.Conclusions: We have demonstrated that peripheral circulating pDCs in patients with SLE were functionally abnormal. They lacked TLR9 expression, were less capable of inducing regulatory T cell differentiation and had persistent IL-10 mRNA expression following the capture of apoptotic PMNs. We suggest circulating pDCs may be pathogenically relevant in SLE. © 2010 Jin et al.; licensee BioMed Central Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/124996
ISSN
2013 Impact Factor: 4.117
2013 SCImago Journal Rankings: 2.194
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
University Grants Council
Government of Hong Kong SAR
Funding Information:

This study was funded by the University Grants Council research grant and The Government of Hong Kong SAR. We thank Miss Ivy Law for her help in drawing blood and Dr. Li-wei Lu and Mr. Otis Ko for their technological suggestions. We thank Miss Helen Law, Dr. Yu-lung Lau and Dr. Eddie Ip for their kind help in the initial stage of setting up the experiments. Thanks are also due to Miss Jessie Wong for her secretarial help and all the subjects who took part in the experiments.

References

 

DC FieldValueLanguage
dc.contributor.authorJin, Oen_HK
dc.contributor.authorKavikondala, Sen_HK
dc.contributor.authorMok, MYen_HK
dc.contributor.authorSun, Len_HK
dc.contributor.authorGu, Jen_HK
dc.contributor.authorFu, Ren_HK
dc.contributor.authorChan, Aen_HK
dc.contributor.authorYeung, Jen_HK
dc.contributor.authorNie, Yen_HK
dc.contributor.authorLau, CSen_HK
dc.date.accessioned2010-10-31T11:05:41Z-
dc.date.available2010-10-31T11:05:41Z-
dc.date.issued2010en_HK
dc.identifier.citationArthritis Research And Therapy, 2010, v. 12 n. 4en_HK
dc.identifier.issn1478-6354en_HK
dc.identifier.urihttp://hdl.handle.net/10722/124996-
dc.description.abstractIntroduction: Dendritic cells (DCs) are capable of inducing immunity or tolerance. Previous studies have suggested plasmacytoid DCs (pDCs) are pathogenic in systemic lupus erythematosus (SLE). However, the functional characteristics of directly isolated peripheral circulating blood pDCs in SLE have not been evaluated previously.Methods: Peripheral blood pDCs from 62 healthy subjects and 58 SLE patients were treated with apoptotic cells derived from polymorphonuclear cells (PMNs). Antigen loaded or unloaded pDCs were then co-cultured with autologous or allogenous T cells. Changes in T cell proliferation, cell surface CD25 expression, intracellular Foxp3 expression and cytokine production were evaluated. pDCs that had captured apoptotic PMNs (pDCs + apoPMNs were also studied for their cytokine production (interferon (IFN)-alpha, interleukin (IL)-6, IL-10, IL-18) and toll like receptor (TLR) expression.Results: Circulating pDCs from SLE patients had an increased ability to stimulate T cells when compared with control pDCs. Using allogenous T cells as responder cells, SLE pDCs induced T cell proliferation even in the absence of apoptotic PMNs. In addition, healthy pDCs + apoPMNs induced suppressive T regulatory cell features with increased Foxp3 expression in CD4 + CD25 + cells while SLE pDCs + apoPMNs did not. There were differences in the cytokine profile of pDCs that had captured apoptotic PMNs between healthy subjects and patients with SLE. Healthy pDCs + apoPMNs showed decreased production of IL-6 but no significant changes in IL-10 and IL-18. These pDCs + apoPMNs also showed increased mRNA transcription of TLR9. On the other hand, while SLE pDCs + apoPMNs also had decreased IL-6, there was decreased IL-18 mRNA expression and persistent IL-10 protein synthesis. In addition, SLE pDCs lacked TLR9 recruitment.Conclusions: We have demonstrated that peripheral circulating pDCs in patients with SLE were functionally abnormal. They lacked TLR9 expression, were less capable of inducing regulatory T cell differentiation and had persistent IL-10 mRNA expression following the capture of apoptotic PMNs. We suggest circulating pDCs may be pathogenically relevant in SLE. © 2010 Jin 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.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.rightsArthritis Research & Therapy. Copyright © BioMed Central Ltd.-
dc.subject.meshAdult-
dc.subject.meshAvian Proteins - metabolism-
dc.subject.meshCell Division - immunology-
dc.subject.meshDendritic Cells - immunology - metabolism - pathology-
dc.subject.meshLupus Erythematosus, Systemic - immunology - pathology-
dc.titleAbnormalities in circulating plasmacytoid dendritic cells in patients with systemic lupus erythematosusen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1478-6354&volume=12&issue=4, article no. R137&spage=&epage=&date=2010&atitle=Abnormalities+in+circulating+plasmacytoid+dendritic+cells+in+patients+with+systemic+lupus+erythematosus-
dc.identifier.emailMok, MY:temy@hkucc.hku.hken_HK
dc.identifier.emailLau, CS:cslau@hku.hken_HK
dc.identifier.authorityMok, MY=rp00490en_HK
dc.identifier.authorityLau, CS=rp01348en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1186/ar3075en_HK
dc.identifier.pmid20618924-
dc.identifier.pmcidPMC2945027-
dc.identifier.scopuseid_2-s2.0-77954339436en_HK
dc.identifier.hkuros195373en_HK
dc.identifier.hkuros174742en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-77954339436&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume12en_HK
dc.identifier.issue4en_HK
dc.identifier.eissn1478-6362-
dc.identifier.isiWOS:000283841500011-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridJin, O=7004432895en_HK
dc.identifier.scopusauthoridKavikondala, S=14819602600en_HK
dc.identifier.scopusauthoridMok, MY=7006024184en_HK
dc.identifier.scopusauthoridSun, L=35265069800en_HK
dc.identifier.scopusauthoridGu, J=8622266500en_HK
dc.identifier.scopusauthoridFu, R=36782017400en_HK
dc.identifier.scopusauthoridChan, A=7403168355en_HK
dc.identifier.scopusauthoridYeung, J=24482785000en_HK
dc.identifier.scopusauthoridNie, Y=15072918200en_HK
dc.identifier.scopusauthoridLau, CS=14035682100en_HK
dc.identifier.citeulike7470065-

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