Journal Article

Diverse intracellular pathogens activate type III interferon expression from peroxisomes

Institute for Medical Engineering and Science ; Massachusetts Institute of Technology (MIT), Interactions Bactéries-Cellules (UIBC) ; Institut National de la Recherche Agronomique (INRA)-Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM), US National Institutes of Health (AI093589 AI072955 P30 DK34854 CA159132 ) ; Burroughs Wellcome Fund ; Crohn's and Colitis Foundation of America ; Agence National de la Recherche (ANR project Mitopatho) ; Erwin Schrodinger Fellowship of the Austrian Science Fund (FWF) ; Herchel Smith Graduate Fellowship Program ; Massachusetts Institute of Technology-Boston Children's Hospital Collaborative grant ; European Research Council Advanced Grant ; Howard Hughes Medical Institute, MICrobiologie de l'ALImentation au Service de la Santé (MICALIS) ; Institut National de la Recherche Agronomique (INRA)-AgroParisTech, Department of Infectious Diseases - Virology Schaller research group at CellNetworks and Deutsches Krebsforsch

2014

Overview

Type I interferon responses are considered the primary means by which viral infections are controlled in mammals. Despite this view, several pathogens activate antiviral responses in the absence of type I interferons. The mechanisms controlling type I interferon-independent responses are undefined. We found that RIG-I like receptors (RLRs) induce type III interferon expression in a variety of human cell types, and identified factors that differentially regulate expression of type I and type III interferons. We identified peroxisomes as a primary site of initiation of type III interferon expression, and revealed that the process of intestinal epithelial cell differentiation upregulates peroxisome biogenesis and promotes robust type III interferon responses in human cells. These findings highlight the importance of different intracellular organelles in specific innate immune responses.

• Publisher: Nature Publishing Group,CCSD,Nature Publishing Group US
• Subject: 13/95 / 14/19 / 631/250/262/2106/2518 / 96/109 / 96/21 / Animals / Antineoplastic Agents - pharmacology / Benzimidazoles - pharmacology / Biomedicine / Cell Differentiation / Cell Line / Cyclohexanes - pharmacology / DEAD Box Protein 58 / DEAD-box RNA Helicases - immunology / Enzyme Inhibitors - pharmacology / Humans / Immune response / Immunity, Innate / Immunology / Infectious Diseases / Interferon / Interferons - biosynthesis / Interferons - immunology / Intestinal Mucosa - cytology / Intestinal Mucosa - immunology / Janus Kinase 2 - antagonists & inhibitors / Janus Kinase 2 - genetics / Life Sciences / Mammals / Mice / p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors / p38 Mitogen-Activated Protein Kinases - genetics / Pathogens / Peroxisomes - immunology / Physiological research / Properties / Pyridones - pharmacology / Receptors, Immunologic / Reoviridae - immunology / Reoviridae Infections - immunology / RNA Interference / RNA, Small Interfering / Signal Transduction - immunology / STAT1 Transcription Factor - antagonists & inhibitors / STAT1 Transcription Factor - immunology / Tyrphostins - pharmacology / Vidarabine - analogs & derivatives / Vidarabine - pharmacology
• ISBN: 0003393230000