Interferon Lambda in the Pathogenesis of Inflammatory Bowel Diseases.
Animals
Apoptosis
/ immunology
Cytokines
/ immunology
Epithelial Cells
/ immunology
Humans
Immunity, Innate
/ immunology
Inflammatory Bowel Diseases
/ immunology
Interferons
/ immunology
Intestinal Mucosa
/ cytology
Models, Immunological
Protein Isoforms
/ immunology
STAT Transcription Factors
/ immunology
Signal Transduction
/ immunology
Tight Junctions
/ immunology
Interferon Lambda
Crohn’s disease (CD)
inflammatory bowel disease (IBD)
interferon lambda (IFN-λ)
intestinal epithelial cell (IEC)
ulcerative colitis (UC)
Journal
Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960
Informations de publication
Date de publication:
2021
2021
Historique:
received:
30
08
2021
accepted:
23
09
2021
entrez:
29
10
2021
pubmed:
30
10
2021
medline:
15
2
2022
Statut:
epublish
Résumé
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.
Identifiants
pubmed: 34712246
doi: 10.3389/fimmu.2021.767505
pmc: PMC8547615
doi:
Substances chimiques
Cytokines
0
Protein Isoforms
0
STAT Transcription Factors
0
Interferons
9008-11-1
Interferon Lambda
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
767505Subventions
Organisme : NIAID NIH HHS
ID : R01 AI130055
Pays : United States
Organisme : NIAID NIH HHS
ID : T32 AI007472
Pays : United States
Informations de copyright
Copyright © 2021 Wallace, Constant and Nice.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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