Loss of Trex1 in Dendritic Cells Is Sufficient To Trigger Systemic AutoimmunityCitation formats

  • External authors:
  • Katrin Peschke
  • Martin Achleitner
  • Kathrin Frenzel
  • Alexander Gerbaulet
  • Servi Remzi Ada
  • Nicolas Zeller
  • Stefan Lienenklaus
  • Mathias Lesche
  • Claire Poulet
  • Ronald Naumann
  • Andreas Dahl
  • Ursula Ravens
  • Claudia Günther
  • Klaus-Peter Knobeloch
  • Marco Prinz
  • Axel Roers
  • Rayk Behrendt

Standard

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; Muller, Werner; Knobeloch, Klaus-Peter; Prinz, Marco; Roers, Axel; Behrendt, Rayk.

In: Journal of immunology (Baltimore, Md. : 1950), Vol. 197, No. 6, 2016, p. 2157-2166.

Research output: Contribution to journalArticle

Harvard

Peschke, K, Achleitner, M, Frenzel, K, Gerbaulet, A, Ada, SR, Zeller, N, Lienenklaus, S, Lesche, M, Poulet, C, Naumann, R, Dahl, A, Ravens, U, Günther, C, Muller, W, Knobeloch, K-P, Prinz, M, Roers, A & Behrendt, R 2016, 'Loss of Trex1 in Dendritic Cells Is Sufficient To Trigger Systemic Autoimmunity' Journal of immunology (Baltimore, Md. : 1950), vol. 197, no. 6, pp. 2157-2166. https://doi.org/10.4049/jimmunol.1600722

APA

Peschke, K., Achleitner, M., Frenzel, K., Gerbaulet, A., Ada, S. R., Zeller, N., ... Behrendt, R. (2016). Loss of Trex1 in Dendritic Cells Is Sufficient To Trigger Systemic Autoimmunity. Journal of immunology (Baltimore, Md. : 1950), 197(6), 2157-2166. https://doi.org/10.4049/jimmunol.1600722

Vancouver

Peschke K, Achleitner M, Frenzel K, Gerbaulet A, Ada SR, Zeller N et al. Loss of Trex1 in Dendritic Cells Is Sufficient To Trigger Systemic Autoimmunity. Journal of immunology (Baltimore, Md. : 1950). 2016;197(6):2157-2166. https://doi.org/10.4049/jimmunol.1600722

Author

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 ; Muller, Werner ; Knobeloch, Klaus-Peter ; Prinz, Marco ; Roers, Axel ; Behrendt, Rayk. / Loss of Trex1 in Dendritic Cells Is Sufficient To Trigger Systemic Autoimmunity. In: Journal of immunology (Baltimore, Md. : 1950). 2016 ; Vol. 197, No. 6. pp. 2157-2166.

Bibtex

@article{5282188cccaf448e9a80805067bae94a,
title = "Loss of Trex1 in Dendritic Cells Is Sufficient To Trigger Systemic Autoimmunity",
abstract = "Defects of the intracellular enzyme 3' repair exonuclease 1 (Trex1) cause the rare autoimmune condition Aicardi-Gouti{\`e}res 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.",
author = "Katrin Peschke and Martin Achleitner and Kathrin Frenzel and Alexander Gerbaulet and Ada, {Servi Remzi} and Nicolas Zeller and Stefan Lienenklaus and Mathias Lesche and Claire Poulet and Ronald Naumann and Andreas Dahl and Ursula Ravens and Claudia G{\"u}nther and Werner Muller and Klaus-Peter Knobeloch and Marco Prinz and Axel Roers and Rayk Behrendt",
note = "Copyright {\circledC} 2016 by The American Association of Immunologists, Inc.",
year = "2016",
doi = "10.4049/jimmunol.1600722",
language = "English",
volume = "197",
pages = "2157--2166",
journal = "Journal of Immunology",
issn = "0022-1767",
publisher = "American Association of Immunologists",
number = "6",

}

RIS

TY - JOUR

T1 - Loss of Trex1 in Dendritic Cells Is Sufficient To Trigger Systemic Autoimmunity

AU - Peschke, Katrin

AU - Achleitner, Martin

AU - Frenzel, Kathrin

AU - Gerbaulet, Alexander

AU - Ada, Servi Remzi

AU - Zeller, Nicolas

AU - Lienenklaus, Stefan

AU - Lesche, Mathias

AU - Poulet, Claire

AU - Naumann, Ronald

AU - Dahl, Andreas

AU - Ravens, Ursula

AU - Günther, Claudia

AU - Muller, Werner

AU - Knobeloch, Klaus-Peter

AU - Prinz, Marco

AU - Roers, Axel

AU - Behrendt, Rayk

N1 - Copyright © 2016 by The American Association of Immunologists, Inc.

PY - 2016

Y1 - 2016

N2 - 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.

AB - 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.

U2 - 10.4049/jimmunol.1600722

DO - 10.4049/jimmunol.1600722

M3 - Article

VL - 197

SP - 2157

EP - 2166

JO - Journal of Immunology

JF - Journal of Immunology

SN - 0022-1767

IS - 6

ER -