Abstract
Toll-like receptors (TLR) and NOD2 are emerging as key mediators of innate host defence in the intestinal mucosa, crucially involved in maintaining mucosal as well as commensal homeostasis. Recent observations suggest new (patho-) physiological mechanisms of how functional versus dysfunctional TLRx/NOD2 pathways may oppose or favour inflammatory bowel disease (IBD). In health, TLRx signalling protects the intestinal epithelial barrier and confers commensal tolerance whereas NOD2 signalling exerts antimicrobial activity and prevents pathogenic invasion. In disease, aberrant TLRx and/or NOD2 signalling may stimulate diverse inflammatory responses leading to acute and chronic intestinal inflammation with many different clinical phenotypes.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Bacteria / genetics
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Bacteria / immunology
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Bacterial Infections / genetics
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Bacterial Infections / immunology*
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Crohn Disease / genetics
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Crohn Disease / immunology
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Genetic Predisposition to Disease / genetics
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Homeostasis / genetics
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Homeostasis / immunology
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Humans
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Immunity, Mucosal
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Inflammatory Bowel Diseases / genetics
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Inflammatory Bowel Diseases / immunology
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Intestinal Mucosa / immunology*
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Intracellular Signaling Peptides and Proteins / genetics
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Intracellular Signaling Peptides and Proteins / immunology*
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Ligands
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Membrane Glycoproteins / genetics
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Membrane Glycoproteins / immunology*
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Nod2 Signaling Adaptor Protein
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Polymorphism, Genetic / genetics
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Polymorphism, Genetic / immunology
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Receptors, Cell Surface / genetics
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Receptors, Cell Surface / immunology*
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Signal Transduction / genetics
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Signal Transduction / immunology
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Toll-Like Receptors
Substances
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Intracellular Signaling Peptides and Proteins
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Ligands
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Membrane Glycoproteins
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NOD2 protein, human
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Nod2 Signaling Adaptor Protein
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Receptors, Cell Surface
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Toll-Like Receptors