Decoy receptor 3 promotes inflammation in Crohn’s disease

Epithelial barrier dysfunction and apoptosis resistance of immune cells have been proposed to contribute to the chronic inflammation seen in patients with inflammatory bowel disease. The soluble decoy receptor 3 (DcR3) inhibits death ligand-induced apoptosis. In the study by Funke and co-writers in this issue of Gut, the authors demonstrate that DcR3 is over-expressed in patients with Crohn’s disease (CD), both in the epithelial layer of ileum (see fig) and in serum. Moreover, this was seen both at active and non-active sites within the gut and present in patients with active and non-active disease. Furthermore, they could also demonstrate that DcR3 over-expression was associated with activation of nuclear factor kappa B (NF-κB), which is of interest because a deregulated activation of NF-κB-dependent pro-survival signalling pathways may be involved in malignant transformation of enterocytes. The increased DcR3 expression was also found to protect against death ligand-induced apoptosis of intestinal epithelial cells and lamina propria T cells. Taken together, this data supports the involvement of DcR3 in the pathogenesis of CD, where it likely promotes inflammation and may also be involved in carcinogenesis.

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