Abstract
The immune system of the gastrointestinal (GI) tract manages the significant task of recognizing and eliminating pathogens while maintaining tolerance of commensal bacteria. Dysregulation of this delicate balance can be detrimental, resulting in severe inflammation, intestinal injury, and cancer. Therefore, mechanisms to relay important signals regulating cell growth and immune reactivity must be in place to support GI homeostasis. Type I interferons (IFN-I) are a family of pleiotropic cytokines, which exert a wide range of biological effects including promotion of both pro- and anti-inflammatory activities. Using animal models of colitis, investigations into the regulation of intestinal epithelium inflammation highlight the role of IFN-I signaling during fine modulation of the immune system. The intestinal epithelium of the gut guides the immune system to differentiate between commensal and pathogenic microbiota, which relies on intimate links with the IFN-I signal-transduction pathway. The current paradigm depicts an IFN-I-induced antiproliferative state in the intestinal epithelium enabling cell differentiation, cell maturation, and proper intestinal barrier function, strongly supporting its role in maintaining baseline immune activity and clearance of damaged epithelia or pathogens. In this review, we will highlight the importance of IFN-I in intestinal homeostasis by discussing its function in inflammation, immunity, and cancer.
Highlights
The Protective Role of Type i interferons in the Gastrointestinal TractUniversity of Colorado Denver School of Medicine, USA Alessandra Mancino, Istituto Europeo di Oncologia, Italy
The gastrointestinal (GI) tract has the greatest mucosal surface area of any organ system shared with the environment, interacting with a wide array of microbes and chemical irritants
Type I interferons are broadly expressed cytokines that drive innate immunity, responding to pathogenic attack or injury with both pro- and anti-inflammatory responses. This remarkable and well-orchestrated task is facilitated by the production of other cytokines and chemokines to eradicate the invading microorganism and begin the process of wound healing
Summary
University of Colorado Denver School of Medicine, USA Alessandra Mancino, Istituto Europeo di Oncologia, Italy. Specialty section: This article was submitted to Molecular Innate Immunity, a section of the journal
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