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10.1038/s41467-017-00573-w

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suck abstract from ncbi


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pmid28874664
      Nat+Commun 2017 ; 8 (1 ): 427
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  • Signalling strength determines proapoptotic functions of STING #MMPMID28874664
  • Gulen MF ; Koch U ; Haag SM ; Schuler F ; Apetoh L ; Villunger A ; Radtke F ; Ablasser A
  • Nat Commun 2017[Sep]; 8 (1 ): 427 PMID28874664 show ga
  • 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.The cGAS/STING signalling pathway is responsible for sensing intracellular DNA and activating downstream inflammatory genes. Here the authors show mouse primary T cells and T leukaemia are hyperresponsive to STING agonist, and this strong STING signalling is associated with apoptosis induction.
  • |*Apoptosis [MESH]
  • |*Signal Transduction [MESH]
  • |Animals [MESH]
  • |Interferon Regulatory Factor-3/metabolism [MESH]
  • |Leukemia, T-Cell/immunology/pathology [MESH]
  • |Membrane Proteins/*metabolism [MESH]
  • |Mice, Inbred C57BL [MESH]
  • |Protein Binding [MESH]
  • |T-Lymphocytes/metabolism [MESH]
  • |Transcription, Genetic [MESH]


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