| Literature DB >> 26275585 |
Antonio Di Sabatino1, Marco Vincenzo Lenti2, Paolo Giuffrida2, Alessandro Vanoli3, Gino Roberto Corazza2.
Abstract
Recent progresses in the immune mechanisms implicated in chronic inflammatory disorders have led to a more in-depth knowledge of the pathogenesis of autoimmune diseases of the gastrointestinal tract, including autoimmune atrophic gastritis, celiac disease, autoimmune enteropathy and ulcerative colitis. While the pathogenic role of specific circulating autoantibodies, i.e., respectively anti-parietal cell, anti-tissue transglutaminase, anti-enterocyte and anti-neutrophil cytoplasmic, is still controversial, some common T-cell mediated mechanisms for inflammation - increase in T helper cell type 1/type 17 pro-inflammatory cytokines- or losing self-tolerance-abnormal regulatory T cell function - are recognized as crucial mediators of the tissue damage causing atrophy of the stomach mucosa in autoimmune atrophic gastritis, villous flattening of the small bowel in celiac disease and autoimmune enteropathy, and mucosal ulceration of the colon in ulcerative colitis. This review deals with novel advances in the immunological bases of the aforementioned autoimmune gastrointestinal disorders, and it also highlights immune mechanisms of progression from chronic inflammation to cancer and implications for new therapeutic targets.Entities:
Keywords: Autoimmune atrophic gastritis; Autoimmune enteropathy; Celiac disease; Cytokine; Ulcerative colitis
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Year: 2015 PMID: 26275585 DOI: 10.1016/j.autrev.2015.08.004
Source DB: PubMed Journal: Autoimmun Rev ISSN: 1568-9972 Impact factor: 9.754