Interferon Lambda in the Pathogenesis of Inflammatory Bowel Diseases

Jonathan W. Wallace, David A. Constant, Timothy J. Nice

Research output: Contribution to journalReview articlepeer-review

12 Scopus citations


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.

Original languageEnglish (US)
Article number767505
JournalFrontiers in immunology
StatePublished - Oct 12 2021


  • Crohn’s disease (CD)
  • inflammatory bowel disease (IBD)
  • interferon lambda (IFN-λ)
  • intestinal epithelial cell (IEC)
  • ulcerative colitis (UC)

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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