The role of cGAS/STING in intestinal immunity.

Authors:
Felix Wottawa, Dora Bordoni, Nathan Baran, Philip Rosenstiel, Konrad Aden
Year of publication:
2021
Volume:
-
Issue:
-
Issn:
0014-2980
Journal title abbreviated:
EUR J IMMUNOL
Journal title long:
European journal of immunology
Impact factor:
4.404
Abstract:
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 signalling. 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 signalling in IBD. Here, we summarize recent findings about the origin and function of STING signalling in the gastrointestinal tract and evolve the hypothesis that disturbed STING signalling might be profoundly interconnected with the pathophysiology of IBD. This article is protected by copyright. All rights reserved.