Differential regulation and function of Fas expression on glial cells

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dc.contributor.authorLee, SJko
dc.contributor.authorZhou, Tko
dc.contributor.authorChoi, Chulheeko
dc.contributor.authorWang, Zko
dc.contributor.authorBenveniste, ENko
dc.date.accessioned2013-03-02T17:45:15Z-
dc.date.available2013-03-02T17:45:15Z-
dc.date.created2012-02-06-
dc.date.created2012-02-06-
dc.date.issued2000-02-
dc.identifier.citationJOURNAL OF IMMUNOLOGY, v.164, no.3, pp.1277 - 1285-
dc.identifier.issn0022-1767-
dc.identifier.urihttp://hdl.handle.net/10203/74774-
dc.description.abstractFas/Apo-1 is a member of the TNF receptor superfamily that signals apoptotic cell death in susceptible target cells. Fas or Fas ligand (FasL)-deficient mice are relatively resistant to the induction of experimental allergic encephalomyelitis, implying the involvement of Fas/FasL in this disease process. We have examined the regulation and function of Fas expression in glial cells (astrocytes and microglia), Fas is constitutively expressed by primary murine microglia at a low level and significantly upregulated by TNF-alpha or IFN-gamma stimulation. Primary astrocytes express high constitutive levels of Fas, which are not further affected by cytokine treatment. In microglia, Fas expression is regulated at the level of mRNA expression; TNF-alpha and IFN-gamma induced Fas mRNA by similar to 20-fold. STAT-1 alpha and NF-kappa B activation are involved in IFN-gamma- or TNF-alpha-mediated Fas up-regulation in microglia, respectively. The cytokine TGF-beta inhibits basal expression of Fas as well as cytokine-mediated Fas expression by microglia, Upon incubation of microglial cells with Fast-expressing cells, similar to 20% of cells underwent Fas-mediated cell death, which increased to similar to 60% when cells were pretreated with either TNF-alpha or IFN-gamma, TGF-beta treatment inhibited Fas-mediated cell death of TNF-alpha- or IFN-gamma-stimulated microglial cells. In contrast, astrocytes are resistant to Fas-mediated cell death, however, ligation of Fas induces expression of the chemokines macrophage inflammatory protein-1 beta (MIP-1 beta), MIP-1 alpha, and MIP-2. These data demonstrate that Fas transmits different signals in the two glial cell populations: a cytotoxic signal in microglia and an inflammatory signal in the astrocyte.-
dc.languageEnglish-
dc.publisherAMER ASSOC IMMUNOLOGISTS-
dc.subjectCENTRAL-NERVOUS-SYSTEM-
dc.subjectEXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS-
dc.subjectEXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS-
dc.subjectTRANSFORMING GROWTH FACTOR-BETA-1-
dc.subjectSIGNALING COMPLEX DISC-
dc.subjectT-CELLS-
dc.subjectINDUCED APOPTOSIS-
dc.subjectFACTOR-BETA-
dc.subjectMULTIPLE-SCLEROSIS-
dc.subjectPROTEIN-KINASE-
dc.titleDifferential regulation and function of Fas expression on glial cells-
dc.typeArticle-
dc.identifier.wosid000084910300019-
dc.identifier.scopusid2-s2.0-0000146587-
dc.type.rimsART-
dc.citation.volume164-
dc.citation.issue3-
dc.citation.beginningpage1277-
dc.citation.endingpage1285-
dc.citation.publicationnameJOURNAL OF IMMUNOLOGY-
dc.contributor.localauthorChoi, Chulhee-
dc.contributor.nonIdAuthorLee, SJ-
dc.contributor.nonIdAuthorZhou, T-
dc.contributor.nonIdAuthorWang, Z-
dc.contributor.nonIdAuthorBenveniste, EN-
dc.type.journalArticleArticle-
dc.subject.keywordPlusCENTRAL-NERVOUS-SYSTEM-
dc.subject.keywordPlusEXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS-
dc.subject.keywordPlusEXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS-
dc.subject.keywordPlusTRANSFORMING GROWTH FACTOR-BETA-1-
dc.subject.keywordPlusSIGNALING COMPLEX DISC-
dc.subject.keywordPlusT-CELLS-
dc.subject.keywordPlusINDUCED APOPTOSIS-
dc.subject.keywordPlusFACTOR-BETA-
dc.subject.keywordPlusMULTIPLE-SCLEROSIS-
dc.subject.keywordPlusPROTEIN-KINASE-
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