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Listeria monocytogenes induces IFNβ expression through an IFI16‐, cGAS‐ and STING‐dependent pathway
Author(s) -
Hansen Kathrine,
Prabakaran Thaneas,
Laustsen Anders,
Jørgensen Sofie E,
Rahbæk Stine H,
Jensen Søren B,
Nielsen Rikke,
Leber Jess H,
Decker Thomas,
Horan Kristy A,
Jakobsen Martin R,
Paludan Søren R
Publication year - 2014
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.15252/embj.201488029
Subject(s) - listeria monocytogenes , biology , listeria , intracellular parasite , microbiology and biotechnology , interferon , intracellular , bacteria , virology , genetics
Abstract 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.