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Blood, 29 January 2009, Vol. 113, No. 5, pp. 1045-1052. Prepublished online as a Blood First Edition Paper on October 29, 2008; DOI 10.1182/blood-2007-10-117861. This Article Full Text Full Text (PDF) Supplemental Figure All Versions of this Article: blood-2007-10-117861v1 113/5/1045    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Lang, P. A. Articles by Lang, K. S. Search for Related Content PubMed PubMed Citation Articles by Lang, P. A. Articles by Lang, K. S. Related Collections Immunobiology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Hematopoietic cell–derived interferon controls viral replication and virus-induced disease Philipp A. Lang13,*, Luisa Cervantes-Barragan4,*, Admar Verschoor1, Alexander A. Navarini1,5, Mike Recher1,6, Marc Pellegrini3, Lukas Flatz1, Andreas Bergthaler1, Kenya Honda7, Burkhard Ludewig4, Pamela S. Ohashi3, and Karl S. Lang1,3 1 Institute of Experimental Immunology, University Hospital of Zurich, Zurich, Switzerland; 2 Institute of Physiology, University of Tubingen, Tubingen, Germany; 3 Campbell Family Institute for Breast Cancer Research, Ontario Cancer Institute, Departments of Medical Biophysics and Immunology, Toronto, ON; 4 Research Department, Kantonal Hospital St Gallen, St Gallen, Switzerland; 5 Department of Dermatology and 6 Institute of Clinical Immunology, University Hospital of Zurich, Zurich, Switzerland; and 7 Laboratory of Immune Regulation, Department of Microbiology and Immunology, Graduate School of Medicine, Osaka University, Osaka, Japan Type I interferon (IFN-I) strongly inhibits viral replication and is a crucial factor in controlling virus infections and diseases. Cellular activation through pattern recognition receptors induces interferon production in a wide variety of hematopoietic and nonhematopoietic cell types, including dendritic cells, fibroblasts, hepatocytes, and cells of neuronal origin. The relative contribution of hematopoietic and nonhematopoietic cells to the overall interferon response is an important issue which has not been fully addressed. Using irf7–/– and wild-type bone marrow chimeras we analyzed the contribution of IFN-I from bone marrow–derived sources in the control of viral infections and immunopathology in mice. We found that during systemic cytopathic virus infection, hematopoietic cells were essential for production of IFN-I, inhibition of viral spread to peripheral organs, and limiting cell damage. In a model of autoimmune diabetes induced by noncytopathic virus infection, hematopoietic cell–derived IFN-I was essential for CD8+ T cell–dependent cytotoxicity in pancreatic β-islet cells and induction of diabetes. These data suggest that during systemic viral infection primarily hematopoietic cell–derived IFN-I controls viral replication and viral-induced disease. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

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