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Open AccessFeature PaperReview

Impact of Autophagy of Innate Immune Cells on Inflammatory Bowel Disease

Department of Gastroenterology and Hepatology, Sapporo Medical University School of Medicine, Sapporo 060-8543, Japan
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Received: 4 December 2018 / Revised: 18 December 2018 / Accepted: 18 December 2018 / Published: 22 December 2018
(This article belongs to the Special Issue Autophagy in Tissue Injury and Homeostasis)
Autophagy, an intracellular degradation mechanism, has many immunological functions and is a constitutive process necessary for maintaining cellular homeostasis and organ structure. One of the functions of autophagy is to control the innate immune response. Many studies conducted in recent years have revealed the contribution of autophagy to the innate immune response, and relationships between this process and various diseases have been reported. Inflammatory bowel disease is an intractable disorder with unknown etiology; however, immunological abnormalities in the intestines are known to be involved in the pathology of inflammatory bowel disease, as is dysfunction of autophagy. In Crohn’s disease, many associations with autophagy-related genes, such as ATG16L1, IRGM, NOD2, and others, have been reported. Abnormalities in the ATG16L1 gene, in particular, have been reported to cause autophagic dysfunction, resulting in enhanced production of inflammatory cytokines by macrophages as well as abnormal function of Paneth cells, which are important in intestinal innate immunity. In this review, we provide an overview of the autophagy mechanism in innate immune cells in inflammatory bowel disease. View Full-Text
Keywords: autophagy; innate immunity; immune cell; inflammasome; Paneth cell; inflammatory bowel disease; Crohn’s disease autophagy; innate immunity; immune cell; inflammasome; Paneth cell; inflammatory bowel disease; Crohn’s disease
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MDPI and ACS Style

Iida, T.; Yokoyama, Y.; Wagatsuma, K.; Hirayama, D.; Nakase, H. Impact of Autophagy of Innate Immune Cells on Inflammatory Bowel Disease. Cells 2019, 8, 7.

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