Signalling strength determines proapoptotic functions of STING
Muhammet F. Gulen,
Ute Koch,
Simone M. Haag,
Fabian Schuler,
Lionel Apetoh,
Andreas Villunger,
Freddy Radtke and
Andrea Ablasser ()
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Muhammet F. Gulen: Ecole Polytechnique Fédérale de Lausanne (EPFL)
Ute Koch: Ecole Polytechnique Fédérale de Lausanne (EPFL)
Simone M. Haag: Ecole Polytechnique Fédérale de Lausanne (EPFL)
Fabian Schuler: Medical University of Innsbruck
Lionel Apetoh: Université de Bourgogne
Andreas Villunger: Medical University of Innsbruck
Freddy Radtke: Ecole Polytechnique Fédérale de Lausanne (EPFL)
Andrea Ablasser: Ecole Polytechnique Fédérale de Lausanne (EPFL)
Nature Communications, 2017, vol. 8, issue 1, 1-10
Abstract:
Abstract Mammalian cells use cytosolic nucleic acid receptors to detect pathogens and other stress signals. In innate immune cells the presence of cytosolic DNA is sensed by the cGAS–STING signalling pathway, which initiates a gene expression programme linked to cellular activation and cytokine production. Whether the outcome of the STING response varies between distinct cell types remains largely unknown. Here we show that T cells exhibit an intensified STING response, which leads to the expression of a distinct set of genes and results in the induction of apoptosis. Of note, this proapoptotic STING response is still functional in cancerous T cells and delivery of small molecule STING agonists prevents in vivo growth of T-cell-derived tumours independent of its adjuvant activity. Our results demonstrate how the magnitude of STING signalling can shape distinct effector responses, which may permit for cell type-adjusted behaviours towards endogenous or exogenous insults.
Date: 2017
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_s41467-017-00573-w
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DOI: 10.1038/s41467-017-00573-w
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