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Type I interferons link viral infection to enhanced epithelial turnover and repair.
Sun, Lulu; Miyoshi, Hiroyuki; Origanti, Sofia; Nice, Timothy J; Barger, Alexandra C; Manieri, Nicholas A; Fogel, Leslie A; French, Anthony R; Piwnica-Worms, David; Piwnica-Worms, Helen; Virgin, Herbert W; Lenschow, Deborah J; Stappenbeck, Thaddeus S.
Afiliação
  • Sun L; Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.
  • Miyoshi H; Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.
  • Origanti S; Department of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, MO 63110, USA.
  • Nice TJ; Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.
  • Barger AC; Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.
  • Manieri NA; Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.
  • Fogel LA; Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Pediatrics, Washington University School of Medicine, St. Louis, MO 63110, USA.
  • French AR; Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Pediatrics, Washington University School of Medicine, St. Louis, MO 63110, USA.
  • Piwnica-Worms D; Department of Cancer Systems Imaging, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
  • Piwnica-Worms H; Department of Cancer Biology, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
  • Virgin HW; Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.
  • Lenschow DJ; Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA; Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
  • Stappenbeck TS; Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. Electronic address: stappenb@pathology.wustl.edu.
Cell Host Microbe ; 17(1): 85-97, 2015 Jan 14.
Article em En | MEDLINE | ID: mdl-25482432
ABSTRACT
The host immune system functions constantly to maintain chronic commensal and pathogenic organisms in check. The consequences of these immune responses on host physiology are as yet unexplored, and may have long-term implications in health and disease. We show that chronic viral infection increases epithelial turnover in multiple tissues, and the antiviral cytokines type I interferons (IFNs) mediate this response. Using a murine model with persistently elevated type I IFNs in the absence of exogenous viral infection, the Irgm1(-/-) mouse, we demonstrate that type I IFNs act through nonepithelial cells, including macrophages, to promote increased epithelial turnover and wound repair. Downstream of type I IFN signaling, the highly related IFN-stimulated genes Apolipoprotein L9a and b activate epithelial proliferation through ERK activation. Our findings demonstrate that the host immune response to chronic viral infection has systemic effects on epithelial turnover through a myeloid-epithelial circuit.
Assuntos

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Viroses / Interferon Tipo I / Células Epiteliais / Epitélio Tipo de estudo: Prognostic_studies Limite: Animals Idioma: En Revista: Cell Host Microbe Ano de publicação: 2015 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Viroses / Interferon Tipo I / Células Epiteliais / Epitélio Tipo de estudo: Prognostic_studies Limite: Animals Idioma: En Revista: Cell Host Microbe Ano de publicação: 2015 Tipo de documento: Article