Spondyloarthropathies (SpA) are commonly observed extra-intestinal manifestations of both Crohn's disease (CD) and ulcerative colitis (UC), the two major forms of inflammatory bowel diseases (IBD). However, the immunological link between these two clinical entities is still poorly understood. Several lines of evidence indicate that SpA may originate from the relocation to the joints of the immune process primarily induced in the gut. The transfer of the intestinal inflammatory process into the joints implicates that immune cells activated in the gut-draining lymph nodes can localize, at a certain point of the intestinal disease, either into the gut or into the joints. This is indicated by the overlapping expression of adhesion molecules observed on the surface of intestinal and synovial endothelial cells during inflammation. Moreover bacterial antigens and HLA-B27 expression may be implicated in the reactivation of T cells at the articular level. Finally, accumulating evidence indicates that a T helper 17 cell-mediated immune response may contribute to IBD and IBD-related SpA with a crucial role played by tumor necrosis factor-alpha in CD and to a lesser extent in UC. (C) 2009 The WJG Press and Baishideng. All rights reserved.

Fantini, M.c., Pallone, F., Monteleone, G. (2009). Common immunologic mechanisms in inflammatory bowel disease and spondylarthropathies. In World Journal of Gastroenterology (pp.2472-2478). BEIJING [10.3748/wjg.15.2472].

Common immunologic mechanisms in inflammatory bowel disease and spondylarthropathies

FANTINI, MASSIMO CLAUDIO;PALLONE, FRANCESCO;MONTELEONE, GIOVANNI
2009-01-01

Abstract

Spondyloarthropathies (SpA) are commonly observed extra-intestinal manifestations of both Crohn's disease (CD) and ulcerative colitis (UC), the two major forms of inflammatory bowel diseases (IBD). However, the immunological link between these two clinical entities is still poorly understood. Several lines of evidence indicate that SpA may originate from the relocation to the joints of the immune process primarily induced in the gut. The transfer of the intestinal inflammatory process into the joints implicates that immune cells activated in the gut-draining lymph nodes can localize, at a certain point of the intestinal disease, either into the gut or into the joints. This is indicated by the overlapping expression of adhesion molecules observed on the surface of intestinal and synovial endothelial cells during inflammation. Moreover bacterial antigens and HLA-B27 expression may be implicated in the reactivation of T cells at the articular level. Finally, accumulating evidence indicates that a T helper 17 cell-mediated immune response may contribute to IBD and IBD-related SpA with a crucial role played by tumor necrosis factor-alpha in CD and to a lesser extent in UC. (C) 2009 The WJG Press and Baishideng. All rights reserved.
Symposium on Inflammatory Bowel Disease
Messina, ITALY
JAN, 2008
Rilevanza internazionale
2009
Settore MED/12 - GASTROENTEROLOGIA
English
adalimumab; bacterial antigen; cell adhesion molecule; etanercept; HLA B27 antigen; infliximab; placebo; tumor necrosis factor alpha; antigen; homing receptor; immunosuppressive agent; antigen expression; article; Crohn disease; disease association; endothelium cell; enteritis; genetic association; human; immune response; immunocompetent cell; immunostimulation; pathogenesis; spondyloarthropathy; ulcerative colitis; animal; cell motion; chemistry; clinical trial; immunology; inflammation; molecular mimicry; pathology; physiology; T lymphocyte; Animals; Antigens; Cell Movement; Clinical Trials as Topic; HLA-B27 Antigen; Humans; Immunosuppressive Agents; Inflammation; Inflammatory Bowel Diseases; Molecular Mimicry; Receptors, Lymphocyte Homing; Spondylarthropathies; T-Lymphocytes
Intervento a convegno
Fantini, M.c., Pallone, F., Monteleone, G. (2009). Common immunologic mechanisms in inflammatory bowel disease and spondylarthropathies. In World Journal of Gastroenterology (pp.2472-2478). BEIJING [10.3748/wjg.15.2472].
Fantini, Mc; Pallone, F; Monteleone, G
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2108/28837
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