| Theme |
Intestinal mucosal immunology update for clinician |
| Title |
Development of inflammatory bowel disease due to impaired innate immune responses |
| Author |
Tomohiro Watanabe |
Center for Innovation in Immunoregulative Technology and Therapeutics, Kyoto University Graduate School of Medicine / Department of Gastroenterology and Hepatology, Kyoto University Graduate School of Medicine |
| Author |
Tsutomu Chiba |
Department of Gastroenterology and Hepatology, Kyoto University Graduate School of Medicine |
| [ Summary ] |
It is now generally accepted that excessive immune reactions towards intestinal microflora underlie the immuno-pathogenesis of inflammatory bowel diseases. Antigens derived from the intestinal microflora activate the host innate immune system via pattern recognition receptors such as Toll-like receptors and nucleotide binding oligomerization-like receptors. Steady-state intestinal immune homeostasis is achieved by negative regulation of host innate immune responses to intestinal microflora. In contrast, dysregulated innate immune responses to intestinal microflora lead to the development of intestinal inflammation due to over-production of pro-inflammatory cytokines or to impaired mucosal host defense. This notion is supported by recent genome-wide association studies which identify mutations in nucleotide binding oligomerization domain 2 or autophagy related 16-like 1 as susceptible gene factors for Crohn's disease. |