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Significance Polymorphisms in NOD2, an intracellular sensor of bacterial peptidoglycan, lead to a significantly increased risk for developing Crohn’s disease. However, the mechanisms by which altered NOD2 function leads to overt intestinal inflammation remain poorly described. Here, we demonstrate a function of NOD2, whereby its activation leads to the generation of immunological tolerance to foreign antigens by inducing tolerant dendritic cells both systemically and within the intestine. This occurs via the generation of the cytokine GM-CSF, a factor that itself has previously been linked to Crohn’s disease development. The identification of a common immunological pathway shared by these two factors will open up new avenues for therapy and further research to identify the precise etiology of this chronic, debilitating condition.

NOD2 modulates immune tolerance via the GM-CSF–dependent generation of CD103+dendritic cells

NOD2 modulates immune tolerance via the GM-CSF–dependent generation of CD103⁺dendritic cells