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Inactivation of Interferon Receptor Promotes the Establishment of Immune Privileged Tumor Microenvironment.
Katlinski, Kanstantsin V; Gui, Jun; Katlinskaya, Yuliya V; Ortiz, Angelíca; Chakraborty, Riddhita; Bhattacharya, Sabyasachi; Carbone, Christopher J; Beiting, Daniel P; Girondo, Melanie A; Peck, Amy R; Puré, Ellen; Chatterji, Priya; Rustgi, Anil K; Diehl, J Alan; Koumenis, Constantinos; Rui, Hallgeir; Fuchs, Serge Y.
Afiliación
  • Katlinski KV; Department of Biomedical Sciences, Mari Lowe Center for Comparative Oncology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
  • Gui J; Department of Biomedical Sciences, Mari Lowe Center for Comparative Oncology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
  • Katlinskaya YV; Department of Biomedical Sciences, Mari Lowe Center for Comparative Oncology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
  • Ortiz A; Department of Biomedical Sciences, Mari Lowe Center for Comparative Oncology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
  • Chakraborty R; Department of Biomedical Sciences, Mari Lowe Center for Comparative Oncology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
  • Bhattacharya S; Department of Biomedical Sciences, Mari Lowe Center for Comparative Oncology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
  • Carbone CJ; Department of Biomedical Sciences, Mari Lowe Center for Comparative Oncology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
  • Beiting DP; Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
  • Girondo MA; Department of Pathology, Medical College of Wisconsin, Milwaukee, WI 53226, USA.
  • Peck AR; Department of Pathology, Medical College of Wisconsin, Milwaukee, WI 53226, USA.
  • Puré E; Department of Biomedical Sciences, Mari Lowe Center for Comparative Oncology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
  • Chatterji P; Division of Gastroenterology, Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
  • Rustgi AK; Division of Gastroenterology, Department of Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
  • Diehl JA; Department of Biochemistry, Hollings Cancer Center, Medical University of South Carolina, Charleston, SC 29425, USA.
  • Koumenis C; Department of Radiation Oncology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
  • Rui H; Department of Pathology, Medical College of Wisconsin, Milwaukee, WI 53226, USA.
  • Fuchs SY; Department of Biomedical Sciences, Mari Lowe Center for Comparative Oncology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Electronic address: syfuchs@upenn.edu.
Cancer Cell ; 31(2): 194-207, 2017 02 13.
Article en En | MEDLINE | ID: mdl-28196594
ABSTRACT
Refractoriness of solid tumors, including colorectal cancers (CRCs), to immunotherapies is attributed to the immunosuppressive tumor microenvironment that protects malignant cells from cytotoxic T lymphocytes (CTLs). We found that downregulation of the type I interferon receptor chain IFNAR1 occurs in human CRC and mouse models of CRC. Downregulation of IFNAR1 in tumor stroma stimulated CRC development and growth, played a key role in formation of the immune-privileged niche, and predicted poor prognosis in human CRC patients. Genetic stabilization of IFNAR1 improved CTL survival and increased the efficacy of the chimeric antigen receptor T cell transfer and PD-1 inhibition. Likewise, pharmacologic stabilization of IFNAR1 suppressed tumor growth providing the rationale for upregulating IFNAR1 to improve anti-cancer therapies.
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Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Neoplasias Colorrectales / Receptor de Interferón alfa y beta Tipo de estudio: Etiology_studies / Prognostic_studies Límite: Animals / Humans Idioma: En Revista: Cancer Cell Asunto de la revista: NEOPLASIAS Año: 2017 Tipo del documento: Article País de afiliación: Estados Unidos
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Texto completo: 1 Banco de datos: MEDLINE Asunto principal: Neoplasias Colorrectales / Receptor de Interferón alfa y beta Tipo de estudio: Etiology_studies / Prognostic_studies Límite: Animals / Humans Idioma: En Revista: Cancer Cell Asunto de la revista: NEOPLASIAS Año: 2017 Tipo del documento: Article País de afiliación: Estados Unidos