Current concepts of the pathogenesis of inflammatory bowel disease.
Authors
Shanahan, FAffiliation
Cork University Hospital, University College Cork, Ireland.Issue Date
2012-02-03T15:16:02ZMeSH
AutoimmunityColitis, Ulcerative/diagnosis/*etiology/pathology
Crohn Disease/diagnosis/*etiology/pathology
Disease Models, Animal
Humans
Intestinal Mucosa/immunology
Neurosecretory Systems/immunology/physiopathology
T-Lymphocytes/immunology
Metadata
Show full item recordCitation
Ir J Med Sci. 1994 Dec;163(12):544-9.Journal
Irish journal of medical sciencePubMed ID
7843934Abstract
Although the cause of inflammatory bowel disease is not known, the pathogenesis involves an immune-mediated tissue damage that is the result of an interaction among genetic predisposing factors, exogenous triggers and endogenous modifying influences. Multiple genes are involved and operate at the level of the immune response and at the target organ. Exogenous triggers include the enteric microflora which might stimulate the mucosal immune system in genetically predisposed individuals. Endogenous modifying factors such as the psychoneuroendocrine system have regulatory effects on the immune system and the inflammatory response, and may influence the course of the disease. While autoimmune phenomena do occur, particularly in ulcerative colitis, there is no evidence that they are directly responsible for the tissue damage. It appears more likely, particularly in Crohn's disease, that tissue injury may occur as an indirect or "bystander" effect of mucosal T-cell hyperactivation, perhaps in response to a normal enteric microbial antigen. Most of the immunologic and histologic features of Crohn's disease can be explained by the effects of T-cell derived and other cytokines on the epithelium, the local immune system, the microvasculature, and the recruitment of auxiliary effector cells such as neutrophils.Language
engISSN
0021-1265 (Print)0021-1265 (Linking)
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