The road to Crohn's disease

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Science  08 Sep 2017:
Vol. 357, Issue 6355, pp. 976-977
DOI: 10.1126/science.aao4158

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Crohn's disease, one of the two main forms of inflammatory bowel disease (IBD), is characterized in most patients by inflammation of the terminal ileum of the small intestine—a site of intense microbe–host engagement. Impairment in the conjoined action of autophagy (a cellular recycling pathway) and the endoplasmic reticulum (ER) stress response (called the unfolded protein response, UPR) within Paneth cells, specialized small intestinal epithelial cells (IECs), can instigate ileal inflammation (1). On page 1047 of this issue, Bel et al. (2) extend this notion by characterizing a mechanism of release of the antimicrobial peptide lysozyme via secretory autophagy from Paneth cells that might contribute to our understanding of how gene variants that affect both the UPR and autophagy predispose to Crohn's disease.

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