Abstract
Interferon λ (IFN-λ) is critical for host viral defense at mucosal surfaces and stimulates immunomodulatory signals, acting on epithelial cells and few other cell types due to restricted IFN-λ receptor expression. Epithelial cells of the intestine play a critical role in the pathogenesis of Inflammatory Bowel Disease (IBD), and the related type II interferons (IFN-γ) have been extensively studied in the context of IBD. However, a role for IFN-λ in IBD onset and progression remains unclear. Recent investigations of IFN-λ in IBD are beginning to uncover complex and sometimes opposing actions, including pro-healing roles in colonic epithelial tissues and potentiation of epithelial cell death in the small intestine. Additionally, IFN-λ has been shown to act through non-epithelial cell types, such as neutrophils, to protect against excessive inflammation. In most cases IFN-λ demonstrates an ability to coordinate the host antiviral response without inducing collateral hyperinflammation, suggesting that IFN-λ signaling pathways could be a therapeutic target in IBD. This mini review discusses existing data on the role of IFN-λ in the pathogenesis of inflammatory bowel disease, current gaps in the research, and therapeutic potential of modulating the IFN-λ-stimulated response.
Highlights
Interferon Lambda in the Pathogenesis of Inflammatory Bowel DiseasesEpithelial cells of the intestine play a critical role in the pathogenesis of Inflammatory Bowel Disease (IBD), and the related type II interferons (IFN-g) have been extensively studied in the context of Inflammatory bowel disease (IBD)
Inflammatory bowel disease (IBD) is the collective term for Ulcerative Colitis (UC) and Crohn’s Disease (CD)
Other recent studies of intestinal inflammation associated with graft versus host disease reported a partial, protective role for hematopoietic expression of Interferon l (IFN-l) receptor that is distinct from promoting epithelial cell proliferation and mucosal healing [58]
Summary
Epithelial cells of the intestine play a critical role in the pathogenesis of Inflammatory Bowel Disease (IBD), and the related type II interferons (IFN-g) have been extensively studied in the context of IBD. In most cases IFN-l demonstrates an ability to coordinate the host antiviral response without inducing collateral hyperinflammation, suggesting that IFN-l signaling pathways could be a therapeutic target in IBD. This mini review discusses existing data on the role of IFN-l in the pathogenesis of inflammatory bowel disease, current gaps in the research, and therapeutic potential of modulating the IFN-l-stimulated response
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