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Epithelial autophagy controls chronic colitis by reducing TNF-induced apoptosis.

Johanna PottKevin J Maloy
Published in: Autophagy (2018)
Genome-wide association studies (GWAS) linking polymorphisms in ATG16L1 with susceptibility to inflammatory bowel disease (IBD) have prompted mucosal immunologists to investigate the functional roles of macroautophagy/autophagy in different cell types in the gut. Here we present a recent study that addressed 2 key questions: in which cell type is autophagy deficiency most detrimental during chronic colitis and what is the functional role of autophagy in those cells? We report that autophagy in intestinal epithelial cells (IECs) acts to limit intestinal inflammation by protecting them from TNF-induced apoptosis and we discuss the potential implications for IBD treatment.
Keyphrases
  • induced apoptosis
  • endoplasmic reticulum stress
  • oxidative stress
  • signaling pathway
  • cell death
  • ulcerative colitis
  • rheumatoid arthritis
  • genome wide association
  • pi k akt
  • stem cells
  • single cell
  • drug induced