Please use this identifier to cite or link to this item: https://www.arca.fiocruz.br/handle/icict/11014
Title: Antagonistic action of IFN-beta and IFN-gamma on high affinity Fc gamma receptor expression in healthy controls and multiple sclerosis patients
Authors: Van Weyenbergh, Johan Jozef Rosa Maria
Lipinski, Pawel
Abadie, Annie
Chabas, Dorothé
Blank, Ulrich
Liblau, Roland
Wietzerbin, Juana
Affilliation: Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, Brasil / nstitut National de la Santé et de la Recherche Médicale (INSERM). Institut Curie. Paris, France
Institut National de la Santé et de la Recherche Médicale (INSERM). Institut Curie. Paris, France
Institut National de la Santé et de la Recherche Médicale (INSERM). Institut Curie. Paris, France
Hôpital Pitié-Salpêtrière. Fédération de Neurologie et INSERM. Laboratoire d’Immunologie Cellulaire. Paris, France
Institut Pasteur. Unité d’Immuno-Allergie. Paris, France
Hôpital Pitié-Salpêtrière. Fédération de Neurologie et INSERM. Laboratoire d’Immunologie Cellulaire. Paris, France
nstitut National de la Santé et de la Recherche Médicale (INSERM). Institut Curie. Paris, France
Abstract: Monocyte-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.
DeCS: Interferon beta/farmacologia
Interferon gama/farmacologia
Esclerose Múltipla/imunologia
Receptores de IgG/antagonistas & inibidores
Receptores de IgG/biossíntese
Adulto
Células Cultivadas
Citocinas/secreção
Relação Dose-Resposta Imunológica
Feminino
Humanos
Líquido Intracelular/imunologia
Masculino
Proteínas de Membrana/antagonistas & inibidores
Meia-Idade
Monócitos/efeitos de drogas
Esclerose Múltipla/genética
RNA Mensageiro/biossíntese
Receptores de IgG/sangue
Explosão Respiratória/efeitos de drogas
Issue Date: 1998
Publisher: American Association of Immunologists
Citation: Antagonistic 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.
ISSN: 0022-1767
Copyright: open access
Appears in Collections:BA - IGM - Artigos de Periódicos

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