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Article: Studies on Fas ligand expression in patients with systemic lupus erythematosus

TitleStudies on Fas ligand expression in patients with systemic lupus erythematosus
Authors
Issue Date1997
Citation
[Hokkaido Igaku Zasshi] The Hokkaido Journal Of Medical Science, 1997, v. 72 n. 4, p. 443-455 How to Cite?
AbstractThe Fas/Fas ligand (FasL)-mediated apoptosis may play a role in the induction and maintenance of T cell tolerance. To investigate the role of FasL in the apoptosis of lymphocytes in autoimmune diseases, gene and protein expression of FasL were examined in peripheral blood mononuclear cells (PBMC) from patients with systemic lupus erythematosus (SLE) or rheumatoid arthritis (RA), and from healthy donors by a newly-designed semiquantitative reverse transcription (RT)-PCR and flow cytometry. Although no significant difference in FasL gene expression was obtained among three groups, SLE patients exhibited a wide distribution of the values. In SLE patients, there was a significant correlation between FasL gene expression by PBMC and some clinical parameters including SLE Disease Activity Index (SLEDAI) score, anti-DNA antibody titer and complement titer (CH50). More interestingly, a marked increase in FasL gene expression was observed in untreated SLE patients, whereas a significant decrease was observed in prednisolone-treated SLE patients. Flow cytometric analysis revealed the expression of FasL on T cell subsets from SLE patients and on anti-CD3 mAb-stimulated T cells from healthy donors. In vitro experiments, dexamethasone inhibited FasL gene expression by PBMC from healthy donors in a dose-dependent manner and with time of incubation. These results clearly indicate that FasL is up-regulated in active SLE patients, reflecting in vivo T cell activation, and that corticosteroids directly down-regulate FasL gene expression by human PBMC.
Persistent Identifierhttp://hdl.handle.net/10722/179402
ISSN
2015 SCImago Journal Rankings: 0.101

 

DC FieldValueLanguage
dc.contributor.authorFeng, Yen_US
dc.date.accessioned2012-12-19T09:56:11Z-
dc.date.available2012-12-19T09:56:11Z-
dc.date.issued1997en_US
dc.identifier.citation[Hokkaido Igaku Zasshi] The Hokkaido Journal Of Medical Science, 1997, v. 72 n. 4, p. 443-455en_US
dc.identifier.issn0367-6102en_US
dc.identifier.urihttp://hdl.handle.net/10722/179402-
dc.description.abstractThe Fas/Fas ligand (FasL)-mediated apoptosis may play a role in the induction and maintenance of T cell tolerance. To investigate the role of FasL in the apoptosis of lymphocytes in autoimmune diseases, gene and protein expression of FasL were examined in peripheral blood mononuclear cells (PBMC) from patients with systemic lupus erythematosus (SLE) or rheumatoid arthritis (RA), and from healthy donors by a newly-designed semiquantitative reverse transcription (RT)-PCR and flow cytometry. Although no significant difference in FasL gene expression was obtained among three groups, SLE patients exhibited a wide distribution of the values. In SLE patients, there was a significant correlation between FasL gene expression by PBMC and some clinical parameters including SLE Disease Activity Index (SLEDAI) score, anti-DNA antibody titer and complement titer (CH50). More interestingly, a marked increase in FasL gene expression was observed in untreated SLE patients, whereas a significant decrease was observed in prednisolone-treated SLE patients. Flow cytometric analysis revealed the expression of FasL on T cell subsets from SLE patients and on anti-CD3 mAb-stimulated T cells from healthy donors. In vitro experiments, dexamethasone inhibited FasL gene expression by PBMC from healthy donors in a dose-dependent manner and with time of incubation. These results clearly indicate that FasL is up-regulated in active SLE patients, reflecting in vivo T cell activation, and that corticosteroids directly down-regulate FasL gene expression by human PBMC.en_US
dc.languageengen_US
dc.relation.ispartof[Hokkaido igaku zasshi] The Hokkaido journal of medical scienceen_US
dc.subject.meshAdulten_US
dc.subject.meshAgeden_US
dc.subject.meshAnti-Inflammatory Agents - Pharmacologyen_US
dc.subject.meshApoptosisen_US
dc.subject.meshDexamethasone - Pharmacologyen_US
dc.subject.meshFas Ligand Proteinen_US
dc.subject.meshFemaleen_US
dc.subject.meshGene Expression Regulation - Drug Effectsen_US
dc.subject.meshHumansen_US
dc.subject.meshLeukocytes, Mononuclear - Metabolismen_US
dc.subject.meshLupus Erythematosus, Systemic - Etiologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMembrane Glycoproteins - Genetics - Metabolism - Physiologyen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshPrednisolone - Pharmacologyen_US
dc.subject.meshT-Lymphocytes - Immunologyen_US
dc.subject.meshUp-Regulationen_US
dc.titleStudies on Fas ligand expression in patients with systemic lupus erythematosusen_US
dc.typeArticleen_US
dc.identifier.emailFeng, Y: yfeng@hku.hken_US
dc.identifier.authorityFeng, Y=rp00466en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid9266252-
dc.identifier.scopuseid_2-s2.0-0031181555en_US
dc.identifier.volume72en_US
dc.identifier.issue4en_US
dc.identifier.spage443en_US
dc.identifier.epage455en_US
dc.identifier.scopusauthoridFeng, Y=24467969600en_US

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