Journal
TRENDS IN IMMUNOLOGY
Volume 32, Issue 4, Pages 171-179Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.it.2011.02.002
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Funding
- National Institute of Health [AR056296, AI088177]
- NIAMS Centers of Excellence for Influenza Research and Surveillance (CEIRS)
- American Lebanese Syrian Associated Charities (ALSAC)
- European Union [256432]
- Fonds voor Wetenschappelijk Onderzoek-Vlaanderen
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Inflammatory bowel diseases (IBD) such as Crohn's disease and ulcerative colitis constitute a major health problem in developed countries. Moreover, IBD predisposes to the development of colorectal cancer. The intracellular NOD-like receptor NIrp3 is rapidly emerging as a crucial regulator of intestinal homeostasis. This innate immune receptor mediates assembly of the inflammasome complex in the presence of microbial ligands, triggering caspase-1 activation and secretion of 1L-1 beta and IL-18. Recent studies suggest that defective NIrp3 inflammasome signaling in the gut contributes to IBD through increased permeability across the epithelial barrier and the induction of detrimental immune responses against invading commensals. Here, we review and discuss recent advances of the role of the NIrp3 inflammasome in colitis and colon tumorigenesis.
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