Journal
EUROPEAN JOURNAL OF IMMUNOLOGY
Volume 51, Issue 4, Pages 785-797Publisher
WILEY
DOI: 10.1002/eji.202048777
Keywords
cGAS; STING; autophagy; type I IFN; Inflammatory bowel disease
Categories
Funding
- BMBF iTREAT project
- DFG CRC 1182 C2
- DFG miTarget [RU 5042]
- BMBF-initiative E:med (Try-IBD) [01ZX1915A]
- EKFS research grant [2019_A09]
- Wilhelm Sander-Stiftung [2019.046.1]
- Projekt DEAL
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The gastrointestinal tract is a complex microenvironment constantly interacting with pathogens. Inflammatory bowel disease (IBD) shares characteristics with STING signaling, potentially involving regulation of the microbiota, autophagy, and cell death. Dysregulation of STING signaling may play a significant role in the pathophysiology of IBD.
The gastrointestinal tract is a highly complex microenvironment under constant interaction with potentially harmful pathogens. Inflammatory bowel disease (IBD) is an archetypical inflammatory disease, in which the intestinal epithelium, defective autophagy, endoplasmic reticulum stress and dysbiosis play a key role. Although no risk-mediating gene variants of STING (TMEM173) have been identified so far, several seminal findings have elucidated a novel understanding of STING in the context of acute and chronic inflammation. STING, an endoplasmic reticulum resident adaptor protein binding cyclic dinucleotides, is a main inducer of type I interferons and canonically involved in antiviral and antibacterial immunity. Recent research has shed light on additional features of STING signaling involved in regulating the microbiota, facilitating autophagy, cell death or ER stress. Importantly, an increasing amount of studies suggests a considerable overlap of IBD pathophysiology and features of STING signaling. Since compelling evidence shows dysregulated type I IFNs in IBD, it is prompting to speculate on the hypothetical role of cGAS/STING/type I IFN signaling in IBD. Here, we summarize recent findings about the origin and function of STING signaling in the gastrointestinal tract and evolve the hypothesis that disturbed STING signaling might be profoundly interconnected with the pathophysiology of IBD.
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