Article

Innate immune defence: NOD2 and autophagy in the pathogenesis of Crohn’s disease

Division of Gastroenterology and Hepatology, University Hospital Basel, Switzerland.
Schweizerische medizinische Wochenschrift (Impact Factor: 1.88). 01/2011; 140:w13135. DOI: 10.4414/smw.2010.13135
Source: PubMed

ABSTRACT Crohn's disease (CD) is a chronic inflammatory disorder of the gut with a poorly understood aetiology. Epidemiological studies suggest that the disease occurs in genetically susceptible individuals as a consequence of defects in mucosal barrier function and disregulated immune recognition of commensal gut flora. Of more than 30 genetic loci associated with CD, two genes with important polymorphisms, encoding the intracellular bacterial sensor NOD2/CARD15 and the autophagic regulator ATG16L1, have gained particular prominence as they suggest an important paradigm of CD pathogenesis. Both proteins exert crucial functions in innate immune defence through intracellular bacterial recognition and destruction of bacteria. This review focuses on the physiological functions of the protein products of both genes and discusses how innate immune defences are linked to autophagic processes through recruitment of ATG16L1 by the bacterial sensor NOD2 at sites of microbial infection.

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Available from: Petr Hruz, May 21, 2014
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    • "It is involved in the innate immune response directed against components of the bacterial cell wall (Hugot et al., 2001). To date, more than 30 variations in this gene have been reported (Hruz and Eckmann, 2011). However, three main genetic variants, in the form of single nucleotide polymorphisms (encoding the p.Arg702Trp and p.Gly908Arg substitutions) and a frameshift polymorphism (p.Leu1007fsinsC)] have been shown to increase the risk for CD in Caucasian populations (Adler et al., 2011; Lesage et al., 2002). "
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