Antagonistic action of IFN-beta and IFN-gamma on high affinity Fc gamma receptor expression in healthy controls and multiple sclerosis patients

dc.creatorVan Weyenbergh, Johan Jozef Rosa Maria
dc.creatorLipinski, Pawel
dc.creatorAbadie, Annie
dc.creatorChabas, Dorothé
dc.creatorBlank, Ulrich
dc.creatorLiblau, Roland
dc.creatorWietzerbin, Juana
dc.date2015-06-30T14:24:03Z
dc.date2015-06-30T14:24:03Z
dc.date1998
dc.date.accessioned2023-09-26T20:13:02Z
dc.date.available2023-09-26T20:13:02Z
dc.identifierAntagonistic action of IFN-beta and IFN-gamma on high affinity Fc gamma receptor expression in healthy controls and multiple sclerosis patients. Journal of Immunology, v. 161, n. 3, p. 1568-1574, 1998.
dc.identifier0022-1767
dc.identifierhttps://www.arca.fiocruz.br/handle/icict/11014
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8851627
dc.descriptionMonocyte-macrophage activation by IFN-g is characterized by a pronounced increase of high affinity Fc receptors for IgG (FcgRI), capable of triggering respiratory burst, phagocytosis, Ab-dependent cytotoxicity, and release of proinflammatory cytokines. In view of the antagonism of IFN-b on IFN-g action, of interest in the chronic inflammatory disorder multiple sclerosis, we examined the possible effect of IFN-b on IFN-g induction of FcgRI gene expression. We found that IFN-b significantly downregulated IFN-g-induced FcgRI surface expression in peripheral blood monocytes from healthy donors, in a dose- and timedependent manner. This down-regulation of FcgRI surface levels did not correspond to a decrease in FcgRI mRNA, suggesting a posttranscriptional effect of IFN-b. Down-regulation of FcgRI surface expression correlated with diminished cellular signaling through FcgRI, since the IFN-g-induced increase in Fcg receptor-triggered respiratory burst was nearly completely abrogated by simultaneous addition of IFN-b. Finally, the same antagonism between both IFNs on FcgRI surface expression was observed in peripheral blood monocytes derived from multiple sclerosis patients; inhibition by IFN-b was even increased (82 6 11%), as compared with healthy controls (67 6 4%). These results may partially help explain the beneficial effect of IFN-b in multiple sclerosis.
dc.formatapplication/pdf
dc.languageeng
dc.publisherAmerican Association of Immunologists
dc.rightsopen access
dc.subjectInterferon beta/farmacologia
dc.subjectInterferon gama/farmacologia
dc.subjectEsclerose Múltipla/imunologia
dc.subjectReceptores de IgG/antagonistas & inibidores
dc.subjectReceptores de IgG/biossíntese
dc.subjectAdulto
dc.subjectCélulas Cultivadas
dc.subjectCitocinas/secreção
dc.subjectRelação Dose-Resposta Imunológica
dc.subjectFeminino
dc.subjectHumanos
dc.subjectLíquido Intracelular/imunologia
dc.subjectMasculino
dc.subjectProteínas de Membrana/antagonistas & inibidores
dc.subjectMeia-Idade
dc.subjectMonócitos/efeitos de drogas
dc.subjectEsclerose Múltipla/genética
dc.subjectRNA Mensageiro/biossíntese
dc.subjectReceptores de IgG/sangue
dc.subjectExplosão Respiratória/efeitos de drogas
dc.titleAntagonistic action of IFN-beta and IFN-gamma on high affinity Fc gamma receptor expression in healthy controls and multiple sclerosis patients
dc.typeArticle


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