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Degree of STING activation is associated with disease outcomes
  1. Qiongyuan Hu1,
  2. Jie Wu1,
  3. Yanhan Ren2,
  4. Xiuwen Wu1,
  5. Lin Gao3,
  6. Gefei Wang1,
  7. Guosheng Gu1,
  8. Huajian Ren1,
  9. Zhiwu Hong1,
  10. Dominic A Slade4,
  11. Jianan Ren1
  1. 1Research Institute of General Surgery, Jinling Hospital, Medical School of Nanjing University, Nanjing, China
  2. 2Chicago Medical School, Rosalind Franklin University of Medicine and Science, North Chicago, Illinois, USA
  3. 3Pancreatic Center, Department of General Surgery, Jinling Hospital, Medical School of Nanjing University, Nanjing, China
  4. 4Department of Surgery, Salford Royal NHS Foundation Trust, Salford, UK
  1. Correspondence to Professor Jianan Ren; jiananr{at}gmail.com

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We read with interest the recent paper by Zhao et al,1 which reported that stimulator of interferon genes (STING) signalling alleviated chronic pancreatitis (CP)-induced inflammation and fibrosis. There is increasing evidence that STING activation could lead to inflammatory response and fibrosis. In our opinion, this contention is associated with three major issues: the form of stimulators that activate STING, the degree of STING activation and the type of immune cell lineages activated STING signalling are able to affect its role in the process of disease.

Self-DNA released from various types of cells during infection or inflammation may stimulate cyclic guanosine monophosphate–adenosine monophosphate (GMP–AMP)  synthase (cGAS)–STING pathway to different degrees. Zhao et al1 did not investigate how STING signalling was activated; however, the amount, manner and rate of DNA release under different ways of cell deaths all played important roles in activating downstream pathways. Additionally, recent reports indicated that the extent of DNA oxidation is a key factor in promoting an enhanced inflammatory …

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