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Loss of Trex1 in Dendritic Cells Is Sufficient To Trigger Systemic Autoimmunity.
Peschke, Katrin; Achleitner, Martin; Frenzel, Kathrin; Gerbaulet, Alexander; Ada, Servi Remzi; Zeller, Nicolas; Lienenklaus, Stefan; Lesche, Mathias; Poulet, Claire; Naumann, Ronald; Dahl, Andreas; Ravens, Ursula; Günther, Claudia; Müller, Werner; Knobeloch, Klaus-Peter; Prinz, Marco; Roers, Axel; Behrendt, Rayk.
Afiliación
  • Peschke K; Institute for Immunology, Faculty of Medicine Carl Gustav Carus, University of Technology, 01307 Dresden, Germany;
  • Achleitner M; Institute for Immunology, Faculty of Medicine Carl Gustav Carus, University of Technology, 01307 Dresden, Germany;
  • Frenzel K; Institute of Neuropathology, University of Freiburg, 79106 Freiburg, Germany;
  • Gerbaulet A; Institute for Immunology, Faculty of Medicine Carl Gustav Carus, University of Technology, 01307 Dresden, Germany;
  • Ada SR; Institute for Immunology, Faculty of Medicine Carl Gustav Carus, University of Technology, 01307 Dresden, Germany;
  • Zeller N; Institute of Neuropathology, University of Freiburg, 79106 Freiburg, Germany;
  • Lienenklaus S; Institute for Laboratory Animal Science, Hannover Medical School, 30625 Hannover, Germany; Institute for Experimental Infection Research, TWINCORE, Centre for Experimental and Clinical Infection Research, 30625 Hannover, Germany;
  • Lesche M; Deep Sequencing Group SFB655, Biotechnology Center, University of Technology, 01307 Dresden, Germany;
  • Poulet C; Department of Pharmacology and Toxicology, Faculty of Medicine Carl Gustav Carus, University of Technology, 01307 Dresden, Germany;
  • Naumann R; Max Planck Institute of Molecular Cell Biology and Genetics, 01307 Dresden, Germany;
  • Dahl A; Deep Sequencing Group SFB655, Biotechnology Center, University of Technology, 01307 Dresden, Germany;
  • Ravens U; Department of Pharmacology and Toxicology, Faculty of Medicine Carl Gustav Carus, University of Technology, 01307 Dresden, Germany;
  • Günther C; Department of Dermatology, Faculty of Medicine Carl Gustav Carus, University of Technology, 01307 Dresden, Germany;
  • Müller W; Faculty of Life Sciences, University of Manchester, Manchester M13 9PL, United Kingdom; and.
  • Knobeloch KP; Institute of Neuropathology, University of Freiburg, 79106 Freiburg, Germany;
  • Prinz M; Institute of Neuropathology, University of Freiburg, 79106 Freiburg, Germany; BIOSS Centre for Biological Signalling Studies, University of Freiburg, 79104 Freiburg, Germany.
  • Roers A; Institute for Immunology, Faculty of Medicine Carl Gustav Carus, University of Technology, 01307 Dresden, Germany;
  • Behrendt R; Institute for Immunology, Faculty of Medicine Carl Gustav Carus, University of Technology, 01307 Dresden, Germany; rayk.behrendt@tu-dresden.de.
J Immunol ; 197(6): 2157-66, 2016 09 15.
Article en En | MEDLINE | ID: mdl-27511730
Defects of the intracellular enzyme 3' repair exonuclease 1 (Trex1) cause the rare autoimmune condition Aicardi-Goutières syndrome and are associated with systemic lupus erythematosus. Trex1(-/-) mice develop type I IFN-driven autoimmunity, resulting from activation of the cytoplasmic DNA sensor cyclic GMP-AMP synthase by a nucleic acid substrate of Trex1 that remains unknown. To identify cell types responsible for initiation of autoimmunity, we generated conditional Trex1 knockout mice. Loss of Trex1 in dendritic cells was sufficient to cause IFN release and autoimmunity, whereas Trex1-deficient keratinocytes and microglia produced IFN but did not induce inflammation. In contrast, B cells, cardiomyocytes, neurons, and astrocytes did not show any detectable response to the inactivation of Trex1. Thus, individual cell types differentially respond to the loss of Trex1, and Trex1 expression in dendritic cells is essential to prevent breakdown of self-tolerance ensuing from aberrant detection of endogenous DNA.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Fosfoproteínas / Células Dendríticas / Autoinmunidad / Exodesoxirribonucleasas Límite: Animals Idioma: En Revista: J Immunol Año: 2016 Tipo del documento: Article

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Asunto principal: Fosfoproteínas / Células Dendríticas / Autoinmunidad / Exodesoxirribonucleasas Límite: Animals Idioma: En Revista: J Immunol Año: 2016 Tipo del documento: Article