Pathogenesis of Crohn's disease.
In the absence of a single initiating aetiological factor, most workers envisage Crohn's disease as the manifestation of poorly regulated immune and inflammatory processes within the gut wall. Initially these responses may arise as a response to common antigens associated with the gut--bacterial products being amongst the most obvious candidates. In genetically predisposed individuals there is overexpression both of local immune response mechanisms in the gut wall (T-cells, B-cells and macrophages) and of systemic inflammatory cells (predominantly polymorphonuclear leukocytes), which are attracted into the inflamed gut through activation of adhesion molecules on the vascular endothelium. As a consequence a large number of pro-inflammatory processes are expressed in the gut wall, inadequately checked by the normal counter-inflammatory processes that should serve to limit inflammation. Defining the relative importance of the individual processes, and identifying critical steps that could be inhibited or enhanced for therapeutic purposes, is a major challenge of Crohn's disease research.
Hodgson
H J
HJ
Imperial College School of Medicine, Division of Medicine, Hammersmith Hospital, London, UK.
D001324:Autoantigens; D001402:B-Lymphocytes / Q000276:immunology; D003424:Crohn Disease / Q000209:etiology* / Q000276:immunology / Q000378:metabolism; D016207:Cytokines / Q000096:biosynthesis; D006801:Humans; D018928:Immunity, Mucosal; D007413:Intestinal Mucosa / Q000276:immunology; D008264:Macrophages / Q000276:immunology; D009504:Neutrophils / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology
D001324:Autoantigens; D016207:Cytokines