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https://www.arca.fiocruz.br/handle/icict/11014
ANTAGONISTIC ACTION OF IFN-BETA AND IFN-GAMMA ON HIGH AFFINITY FC GAMMA RECEPTOR EXPRESSION IN HEALTHY CONTROLS AND MULTIPLE SCLEROSIS PATIENTS
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
Autor(es)
Afiliação
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
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
Resumo em Inglês
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/farmacologiaInterferon 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
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