Fisiopatología y complicaciones en la Enfermedad Celíaca
Pathophysiology and complications in celiac disease
Abstract
Celiac disease is an immune-mediated systemic process caused by gluten consumption in genetically susceptible people (HLA-DQ2/DQ8 haplotype) with or without enteropathy. Gluten consumption is the most important environmental trigger. The article describes the environmental, genetic and immune factors that contribute to intestinal pathology and injury. Mechanisms of immunity have been studied and it is currently accepted that adaptive immunity involves the participation of gluten-reactive CD4+ T lymphocytes, which leads to a proinflammatory response dominated by the production of interferon (IFN-γ) and interleukin-21 ( IL-21). In parallel, gluten peptides with incomplete digestion exert a toxic effect with active transepithelial transport, in this case innate immunity activates epithelial cytotoxicity mediated by intraepithelial lymphocytes (IEL). It is important to mention that transglutaminase 2 (TG2) exerts functions as a deamidating enzyme, which can improve the immunostimulatory effect of gluten, and the other as a target autoantigen in the immune response. The pathophysiology of CD is complex, many of the mechanisms involved are still being studied.
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