INTESTINE Vol.15 No.5(5)

Theme Intestinal mucosal immunology update for clinician
Title Involvement of anti-microbial peptide dysfunction in IBD pathogenesis
Publish Date 2011/09
Author Takahiro Ito Division of Gastroenterology and Hematology / Oncology, Department of Medicine, Asahikawa Medical University
Author Mikihiro Fujiya Division of Gastroenterology and Hematology / Oncology, Department of Medicine, Asahikawa Medical University
Author Kentaro Moriichi Division of Gastroenterology and Hematology / Oncology, Department of Medicine, Asahikawa Medical University
Author Kotaro Okamoto Division of Gastroenterology and Hematology / Oncology, Department of Medicine, Asahikawa Medical University
Author Hiroki Tanabe Division of Gastroenterology and Hematology / Oncology, Department of Medicine, Asahikawa Medical University
Author Atsuo Maemoto IBD Center, Sapporo Higashi Tokushukai Hospital
Author Toshifumi Ashida IBD Center, Sapporo Higashi Tokushukai Hospital
Author Tokiyoshi Ayabe Innate Immunity Laboratory, Department of Cellular Life Science, Faculty of Advanced Life Science, Hokkaido University
Author Yutaka Kohgo Division of Gastroenterology and Hematology / Oncology, Department of Medicine, Asahikawa Medical University
[ Summary ] Paneth cells play a central role in intestinal innate immunity through the secretion of anti-microbial peptides. The expression of α-defensin, an anti-microbial peptide, is known to decrease in patients with Crohn's disease. This suggests the significance of altered anti-microbial peptide functions in the etiology of inflammatory bowel disease (IBD). α-defensin exhibits anti-microbial activity, while also enhancing the migration of immature dendritic cells. It also aids induction of the secretion of interleukin-8 from the intestinal epithelia. These actions contribute to the regulation of acquired immunity. This review describes the detailed function of anti-microbial peptides in innate and acquired immunity. It also offers novel insights into the involvement of anti-microbial peptide dysfunction in the pathogenesis of IBD.
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