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Article: An essential protective role of IL-10 in the immunological mechanism underlying resistance vs susceptibility to lupus induction by dendritic cells and dying cells

TitleAn essential protective role of IL-10 in the immunological mechanism underlying resistance vs susceptibility to lupus induction by dendritic cells and dying cells
Authors
Issue Date2011
PublisherOxford University Press. The Journal's web site is located at http://rheumatology.oxfordjournals.org/
Citation
Rheumatology, 2011, v. 50 n. 10, p. 1773-1784 How to Cite?
AbstractObjective: To define the role of IL-10 in lupus pathogenesis, and to understand the immunological mechanisms underlying resistance vs susceptibility to lupus disease induction by dendritic cells (DCs) and dying cells. Methods: Groups of IL-10-deficient and normal C57BL/6 mice were injected with syngenic DCs that had ingested necrotic cells prepared by either freeze-thaw cycle (DC/necF/T) or heat shock (DC/necH/S) procedures, or with DC or necrotic cells alone, or with PBS only. Disease development, including proteinuria and renal pathological changes, was monitored. Levels of autoantibodies against different lupusassociated nuclear antigens were measured by ELISAs, and IC deposition in the kidneys was confirmed by immunostaining. Results: No significant proteinuria was detected in the mice. However, striking renal pathological changes typical of IC-mediated GN were consistently observed in the DC/necF/T-treated IL-10-/- mice. These included glomerular hypercellularity and macrophage infiltration, renal IC deposition, circulating kidneyreactive autoantibodies and the presence of immunoglobulin G2 isotype-specific antibody complexes in the diseased kidneys. We demonstrated further that host-derived IL-10 was primarily responsible for protecting against the induction of pathogenic Th1 type of autoantibody responses in the mice. Conclusion: IL-10 protects against the induction of lupus-like renal end-organ damage by downregulating pathogenic Th1 responses. © The Author(s) 2011. Published by Oxford University Press on behalf of The British Society for Rheumatology on behalf of the British Society for Rheumatology.
Persistent Identifierhttp://hdl.handle.net/10722/170458
ISSN
2015 Impact Factor: 4.524
2015 SCImago Journal Rankings: 1.449
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLing, GSen_US
dc.contributor.authorCook, HTen_US
dc.contributor.authorBotto, Men_US
dc.contributor.authorLau, YLen_US
dc.contributor.authorHuang, FPen_US
dc.date.accessioned2012-10-30T06:09:06Z-
dc.date.available2012-10-30T06:09:06Z-
dc.date.issued2011en_US
dc.identifier.citationRheumatology, 2011, v. 50 n. 10, p. 1773-1784en_US
dc.identifier.issn1462-0324en_US
dc.identifier.urihttp://hdl.handle.net/10722/170458-
dc.description.abstractObjective: To define the role of IL-10 in lupus pathogenesis, and to understand the immunological mechanisms underlying resistance vs susceptibility to lupus disease induction by dendritic cells (DCs) and dying cells. Methods: Groups of IL-10-deficient and normal C57BL/6 mice were injected with syngenic DCs that had ingested necrotic cells prepared by either freeze-thaw cycle (DC/necF/T) or heat shock (DC/necH/S) procedures, or with DC or necrotic cells alone, or with PBS only. Disease development, including proteinuria and renal pathological changes, was monitored. Levels of autoantibodies against different lupusassociated nuclear antigens were measured by ELISAs, and IC deposition in the kidneys was confirmed by immunostaining. Results: No significant proteinuria was detected in the mice. However, striking renal pathological changes typical of IC-mediated GN were consistently observed in the DC/necF/T-treated IL-10-/- mice. These included glomerular hypercellularity and macrophage infiltration, renal IC deposition, circulating kidneyreactive autoantibodies and the presence of immunoglobulin G2 isotype-specific antibody complexes in the diseased kidneys. We demonstrated further that host-derived IL-10 was primarily responsible for protecting against the induction of pathogenic Th1 type of autoantibody responses in the mice. Conclusion: IL-10 protects against the induction of lupus-like renal end-organ damage by downregulating pathogenic Th1 responses. © The Author(s) 2011. Published by Oxford University Press on behalf of The British Society for Rheumatology on behalf of the British Society for Rheumatology.en_US
dc.languageengen_US
dc.publisherOxford University Press. The Journal's web site is located at http://rheumatology.oxfordjournals.org/en_US
dc.relation.ispartofRheumatologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAntibodies, Antinuclear - Blood - Immunologyen_US
dc.subject.meshApoptosis - Immunologyen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshCoculture Techniquesen_US
dc.subject.meshDendritic Cells - Immunology - Metabolism - Pathologyen_US
dc.subject.meshDisease Models, Animalen_US
dc.subject.meshDisease Susceptibility - Immunologyen_US
dc.subject.meshDown-Regulationen_US
dc.subject.meshImmunity, Innate - Immunologyen_US
dc.subject.meshInterleukin-10 - Deficiency - Physiologyen_US
dc.subject.meshKidney - Immunology - Pathologyen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Inbred C57blen_US
dc.subject.meshMice, Inbred Mrl Lpren_US
dc.subject.meshMice, Knockouten_US
dc.subject.meshNecrosisen_US
dc.subject.meshProteinuria - Immunology - Pathologyen_US
dc.subject.meshTh1 Cells - Immunologyen_US
dc.titleAn essential protective role of IL-10 in the immunological mechanism underlying resistance vs susceptibility to lupus induction by dendritic cells and dying cellsen_US
dc.typeArticleen_US
dc.identifier.emailLau, YL:lauylung@hkucc.hku.hken_US
dc.identifier.authorityLau, YL=rp00361en_US
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.doi10.1093/rheumatology/ker198en_US
dc.identifier.pmid21727182en_US
dc.identifier.pmcidPMC3176714-
dc.identifier.scopuseid_2-s2.0-80053159908en_US
dc.identifier.hkuros234986-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-80053159908&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume50en_US
dc.identifier.issue10en_US
dc.identifier.spage1773en_US
dc.identifier.epage1784en_US
dc.identifier.isiWOS:000295172600008-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridLing, GS=24577720400en_US
dc.identifier.scopusauthoridCook, HT=7201617760en_US
dc.identifier.scopusauthoridBotto, M=7004466418en_US
dc.identifier.scopusauthoridLau, YL=7201403380en_US
dc.identifier.scopusauthoridHuang, FP=35358178100en_US

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