Immunopathogenesis of inflammatory bowel disease.
Crohn's disease and ulcerative colitis are chronic relapsing immune mediated disorders that results from an aberrant response to gut luminal antigen in genetically susceptible host. The adaptive immune response that is then triggered was widely considered to be a T-helper-1 mediated condition in Crohn's disease and T-helper-2 mediated condition in ulcerative colitis. Recent studies in animal models, genome wide association, and basic science has provided important insights in in the immunopathogenesis of inflammatory bowel disease, one of which was the characterization of the interleukin-23/Th-17 axis.
Shih
David Q
DQ
Cedars-Sinai Inflammatory Bowel Disease Center, 8700 Beverly Blvd., Los Angeles, CA 90048, USA.
Targan
Stephan R
SR
D000818:Animals; D053468:CARD Signaling Adaptor Proteins / Q000235:genetics / Q000378:metabolism; D004847:Epithelial Cells / Q000166:cytology / Q000378:metabolism; D006801:Humans; D007113:Immunity, Innate / Q000502:physiology; D015212:Inflammatory Bowel Diseases / Q000209:etiology / Q000276:immunology / Q000473:pathology; D020381:Interleukin-17 / Q000276:immunology; D053759:Interleukin-23 / Q000276:immunology; D007413:Intestinal Mucosa / Q000166:cytology / Q000382:microbiology / Q000473:pathology; D013601:T-Lymphocytes / Q000276:immunology; D051193:Toll-Like Receptors / Q000235:genetics / Q000378:metabolism
D053468:CARD Signaling Adaptor Proteins; D020381:Interleukin-17; D053759:Interleukin-23; D051193:Toll-Like Receptors