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Article: Impaired production of IL-12 in systemic lupus erythematosus. III: Deficient IL-12 p40 gene expression and cross-regulation of IL-12, IL-10 and IFN-γ gene expression

TitleImpaired production of IL-12 in systemic lupus erythematosus. III: Deficient IL-12 p40 gene expression and cross-regulation of IL-12, IL-10 and IFN-γ gene expression
Authors
Issue Date1999
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/cytokine
Citation
Cytokine, 1999, v. 11 n. 10, p. 805-811 How to Cite?
AbstractInterleukin 12 (IL-12) is a heterodimer comprising p35 and p40 subunits which are encoded and regulated separately. The authors previously demonstrated deficient IL-12 production in SLE which correlates negatively with disease activity. The present study was designed to determine whether deficiency of IL-12 and excess production of IL-10 and IL-6 in systemic lupus erythematosus (SLE) are due to aberrant regulation at the gene level. Using semiquantitative RT-PCR assay, it was shown that constitutive expression of IL-12 p35 gene is somewhat impaired in SLE compared with controls and that IL-12 p40 mRNA, which was present at low levels in controls, was undetectable in unstimulated SLE peripheral blood mononuclear cells (PBMC). Gene expression of IL-12 p35 and p40 was significantly increased in response to SAC, with significantly lower SAC-induced expression of p40 in SLE patients than controls. SAC-stimulated IL-12 p35 and p40 mRNAs were significantly augmented by interferon γ (IFN-γ). Exogenous IL-12 or IFN-γ significantly inhibited IL-10 gene expression, without affecting IL-6 mRNA or other proinflammatory cytokine mRNA levels. These observations were further confirmed by studies of protein production at the single cell level using ELISPOT assay. Downregulation of IL-12 p40 expression appears to be the cause of IL-12 p70 deficiency in SLE. If this defect could be repaired, normalization of IL-12 and IFN-γ production should reduce excessive IL-10 and prevent pathology.
Persistent Identifierhttp://hdl.handle.net/10722/148150
ISSN
2015 Impact Factor: 2.94
2015 SCImago Journal Rankings: 1.294
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLiu, TFen_US
dc.contributor.authorJones, BMen_US
dc.contributor.authorWong, RWSen_US
dc.contributor.authorSrivastava, Gen_US
dc.date.accessioned2012-05-29T06:11:07Z-
dc.date.available2012-05-29T06:11:07Z-
dc.date.issued1999en_US
dc.identifier.citationCytokine, 1999, v. 11 n. 10, p. 805-811en_US
dc.identifier.issn1043-4666en_US
dc.identifier.urihttp://hdl.handle.net/10722/148150-
dc.description.abstractInterleukin 12 (IL-12) is a heterodimer comprising p35 and p40 subunits which are encoded and regulated separately. The authors previously demonstrated deficient IL-12 production in SLE which correlates negatively with disease activity. The present study was designed to determine whether deficiency of IL-12 and excess production of IL-10 and IL-6 in systemic lupus erythematosus (SLE) are due to aberrant regulation at the gene level. Using semiquantitative RT-PCR assay, it was shown that constitutive expression of IL-12 p35 gene is somewhat impaired in SLE compared with controls and that IL-12 p40 mRNA, which was present at low levels in controls, was undetectable in unstimulated SLE peripheral blood mononuclear cells (PBMC). Gene expression of IL-12 p35 and p40 was significantly increased in response to SAC, with significantly lower SAC-induced expression of p40 in SLE patients than controls. SAC-stimulated IL-12 p35 and p40 mRNAs were significantly augmented by interferon γ (IFN-γ). Exogenous IL-12 or IFN-γ significantly inhibited IL-10 gene expression, without affecting IL-6 mRNA or other proinflammatory cytokine mRNA levels. These observations were further confirmed by studies of protein production at the single cell level using ELISPOT assay. Downregulation of IL-12 p40 expression appears to be the cause of IL-12 p70 deficiency in SLE. If this defect could be repaired, normalization of IL-12 and IFN-γ production should reduce excessive IL-10 and prevent pathology.en_US
dc.languageengen_US
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/cytokineen_US
dc.relation.ispartofCytokineen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshDimerizationen_US
dc.subject.meshGene Expression Regulation - Drug Effectsen_US
dc.subject.meshHumansen_US
dc.subject.meshInterferon-Gamma - Analysis - Genetics - Pharmacologyen_US
dc.subject.meshInterleukin-10 - Analysis - Geneticsen_US
dc.subject.meshInterleukin-12 - Analysis - Chemistry - Genetics - Pharmacologyen_US
dc.subject.meshLeukocytes, Mononuclear - Drug Effects - Immunology - Metabolism - Pathologyen_US
dc.subject.meshLupus Erythematosus, Systemic - Genetics - Immunology - Metabolism - Pathologyen_US
dc.subject.meshMolecular Weighten_US
dc.subject.meshRna, Messenger - Genetics - Metabolismen_US
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_US
dc.subject.meshStaphylococcus Aureus - Immunologyen_US
dc.titleImpaired production of IL-12 in systemic lupus erythematosus. III: Deficient IL-12 p40 gene expression and cross-regulation of IL-12, IL-10 and IFN-γ gene expressionen_US
dc.typeArticleen_US
dc.identifier.emailSrivastava, G: gopesh@pathology.hku.hken_US
dc.identifier.authoritySrivastava, G=rp00365en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1006/cyto.1999.0512en_US
dc.identifier.pmid10525320-
dc.identifier.scopuseid_2-s2.0-0032862515en_US
dc.identifier.hkuros52627-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0032862515&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume11en_US
dc.identifier.issue10en_US
dc.identifier.spage805en_US
dc.identifier.epage811en_US
dc.identifier.isiWOS:000082855700011-
dc.publisher.placeUnited Kingdomen_US
dc.customcontrol.immutablesml 130621-

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