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Increasing evidence suggests that a deficit in innate immunity may play a causative role in the pathogenesis of inflammatory bowel disease. The most compelling support for this hypothesis comes from the genetic association of Crohn disease (CD) with carriage of polymorphisms within the NOD2 gene, which represent the most frequent genetic defect in CD. Our findings suggest that SAMP1/YitFc mice, which develop CD-like ileitis in the absence of NOD2 genetic mutations, fail to respond to MDP administration by displaying decreased innate cytokine production and impaired bacterial clearance before the onset of disease. This provides evidence that dysregulated NOD2 signaling, genetic or functional in nature, predisposes to chronic intestinal inflammation, and supports a new paradigm that CD may occur from a deficit in innate immunity as opposed to an overly aggressive immune response. This new paradigm could lead to potential development of new preventative or therapeutic modalities for patients with CD.

Original publication




Journal article


Gut Microbes

Publication Date





340 - 344


Crohn disease, SAMP/YitFc, inflammatory bowel disease, innate immunity, nucleotide-binding oligomerization domain 2, Animals, Crohn Disease, Disease Models, Animal, Humans, Immunologic Deficiency Syndromes, Mice, Nod2 Signaling Adaptor Protein, Signal Transduction