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Type I Interferon in Chronic Virus Infection and Cancer.
Snell, Laura M; McGaha, Tracy L; Brooks, David G.
Afiliação
  • Snell LM; Princess Margaret Cancer Center, Tumor Immunotherapy Program, University Health Network, Toronto, ONT, M5G 2M9, Canada.
  • McGaha TL; Princess Margaret Cancer Center, Tumor Immunotherapy Program, University Health Network, Toronto, ONT, M5G 2M9, Canada; Department of Immunology, University of Toronto, Toronto, ONT, M5S 1A8, Canada. Electronic address: tmcgaha@uhnresearch.ca.
  • Brooks DG; Princess Margaret Cancer Center, Tumor Immunotherapy Program, University Health Network, Toronto, ONT, M5G 2M9, Canada; Department of Immunology, University of Toronto, Toronto, ONT, M5S 1A8, Canada. Electronic address: dbrooks@uhnresearch.ca.
Trends Immunol ; 38(8): 542-557, 2017 08.
Article em En | MEDLINE | ID: mdl-28579323
Type I interferons (IFN-Is) are emerging as key drivers of inflammation and immunosuppression in chronic infection. Control of these infections requires IFN-I signaling; however, prolonged IFN-I signaling can lead to immune dysfunction. IFN-Is are also emerging as double-edged swords in cancer, providing necessary inflammatory signals, while initiating feedback suppression in both immune and cancer cells. Here, we review the proinflammatory and suppressive mechanisms potentiated by IFN-Is during chronic virus infections and discuss the similar, newly emerging dichotomy in cancer. We then discuss how this understanding is leading to new therapeutic concepts and immunotherapy combinations. We propose that, by modulating the immune response at its foundation, it may be possible to widely reshape immunity to control these chronic diseases.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Viroses / Transdução de Sinais / Interferon Tipo I / Neoplasias Tipo de estudo: Etiology_studies Limite: Animals / Humans Idioma: En Ano de publicação: 2017 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Viroses / Transdução de Sinais / Interferon Tipo I / Neoplasias Tipo de estudo: Etiology_studies Limite: Animals / Humans Idioma: En Ano de publicação: 2017 Tipo de documento: Article