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TY - JOUR AU - Saitoh, Tatsuya AU - Fujita, Naonobu AU - Jang, Myoung Ho AU - Uematsu, Satoshi AU - Yang, Bo-Gie AU - Satoh, Takashi AU - Omori, Hiroko AU - Noda, Takeshi AU - Yamamoto, Naoki AU - Komatsu, Masaaki AU - Tanaka, Keiji AU - Kawai, Taro AU - Tsujimura, Tohru AU - Takeuchi, Osamu AU - Yoshimori, Tamotsu AU - Akira, Shizuo PY - 2008 DA - 2008/11/01 TI - Loss of the autophagy protein Atg16L1 enhances endotoxin-induced IL-1β production JO - Nature SP - 264 EP - 268 VL - 456 IS - 7219 AB - Crohn's disease, a chronic inflammation of the gut, has been linked to over thirty gene loci. Two papers in this issue focus a recent addition to that list, ATG16L1 (Atg16-like 1). Atg16 protein itself was first identified in yeast as an essential gene for the process of autophagy, a system that clears away unwanted cellular components and is involved in the pathogenesis of microbial infection, neurodegeneration and tumorigenesis. Cadwell et al. report a unique role for Atg16L1 in Paneth cells, a type of epithelial cell that secretes granules containing antimicrobial peptides into the intestines. Saitoh et al. show that ATG16L1 plays a role in the inflammatory response in isolated macrophages and in the mouse intestine, as an essential component of the autophagic machinery. This work implicates Atg16L1 in the control of inflammatory immune response and the maintenance of intestinal barrier, both of which are important for the prevention of inflammatory bowel disease. SN - 1476-4687 UR - https://doi.org/10.1038/nature07383 DO - 10.1038/nature07383 ID - Saitoh2008 ER -