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    Current concepts of the pathogenesis of inflammatory bowel disease.

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    Authors
    Shanahan, F
    Affiliation
    Cork University Hospital, University College Cork, Ireland.
    Issue Date
    2012-02-03T15:16:02Z
    MeSH
    Autoimmunity
    Colitis, Ulcerative/diagnosis/*etiology/pathology
    Crohn Disease/diagnosis/*etiology/pathology
    Disease Models, Animal
    Humans
    Intestinal Mucosa/immunology
    Neurosecretory Systems/immunology/physiopathology
    T-Lymphocytes/immunology
    
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    Citation
    Ir J Med Sci. 1994 Dec;163(12):544-9.
    Journal
    Irish journal of medical science
    URI
    http://hdl.handle.net/10147/209243
    PubMed ID
    7843934
    Abstract
    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
    eng
    ISSN
    0021-1265 (Print)
    0021-1265 (Linking)
    Collections
    Cork University Hospital

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