Listeria monocytogenes induces IFNβ expression through an IFI16-, cGAS- and STING-dependent pathway

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  • Kathrine Hansen, Department of Biomedicine, Aarhus University, Aarhus, Denmark Aarhus Research Centre for Innate Immunology, Aarhus University, Aarhus, Denmark., Danmark
  • Thaneas Prabakaran
  • Anders Laustsen
  • Sofie E Jørgensen
  • Stine Hess Rahbek
  • Søren B Jensen, Department of Biomedicine, Aarhus University, Aarhus, Denmark Aarhus Research Centre for Innate Immunology, Aarhus University, Aarhus, Denmark., Danmark
  • Rikke Nielsen
  • Jess H Leber, Department of Microbiology, The University of Chicago, Chicago, IL, USA., Ukendt
  • Thomas Decker, Max F. Perutz Laboratories, Department of Microbiology, Immunobiology and Genetics, University of Vienna, Vienna, Austria., Ukendt
  • Kristy A Horan, Department of Biomedicine, Aarhus University, Aarhus, Denmark., Danmark
  • Martin R Jakobsen
  • Søren R Paludan

Listeria monocytogenes is a gram-positive facultative intracellular bacterium, which replicates in the cytoplasm of myeloid cells. Interferon β (IFNβ) has been reported to play an important role in the mechanisms underlying Listeria disease. Although studies in murine cells have proposed the bacteria-derived cyclic-di-AMP to be the key bacterial immunostimulatory molecule, the mechanism for IFNβ expression during L. monocytogenes infection in human myeloid cells remains unknown. Here we report that in human macrophages, Listeria DNA rather than cyclic-di-AMP is stimulating the IFN response via a pathway dependent on the DNA sensors IFI16 and cGAS as well as the signalling adaptor molecule STING. Thus, Listeria DNA is a major trigger of IFNβ expression in human myeloid cells and is sensed to activate a pathway dependent on IFI16, cGAS and STING.

OriginalsprogEngelsk
TidsskriftE M B O Journal
Vol/bind33
Nummer15
Sider (fra-til)1654-66
Antal sider13
ISSN0261-4189
DOI
StatusUdgivet - 1 aug. 2014

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