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. |