Loss of the autophagy protein Atg16L1 enhances endotoxin-induced IL-1β production View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2008-10-05

AUTHORS

Tatsuya Saitoh, Naonobu Fujita, Myoung Ho Jang, Satoshi Uematsu, Bo-Gie Yang, Takashi Satoh, Hiroko Omori, Takeshi Noda, Naoki Yamamoto, Masaaki Komatsu, Keiji Tanaka, Taro Kawai, Tohru Tsujimura, Osamu Takeuchi, Tamotsu Yoshimori, Shizuo Akira

ABSTRACT

Inflammatory bowel diseaseCrohn'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. More... »

PAGES

264-268

Journal

TITLE

Nature

ISSUE

7219

VOLUME

456

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/nature07383

DOI

http://dx.doi.org/10.1038/nature07383

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1042952038

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/18849965


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