Abstract
Celiac disease (CD) is an immune-mediated enteropathy, triggered by dietary wheat gluten and similar proteins of barley and rye in genetically susceptible individuals. This is a complex disorder involving both environmental and immune-genetic factors. The major genetic risk factor for CD is determined by HLA-DQ genes. Dysfunction of the innate and adaptive immune systems can conceivably cause impairment of mucosal barrier function and development of localized or systemic inflammatory and autoimmune processes. Exposure to gluten is the main environmental trigger responsible for the signs and symptoms of the disease, but exposure to gluten does not fully explain the manifestation of CD. Thus, both genetic determination and environmental exposure to gluten are necessary for the full manifestation of CD; neither of them is sufficient alone. Epidemiological and clinical data suggest that other environmental factors, including infections, alterations in the intestinal microbiota composition, and early feeding practices, might also play a role in disease development. Thus, this interaction is the condicio sine qua non celiac disease can develop. The breakdown of the interaction among microbiota, innate immunity, and genetic and dietary factors leads to disruption of homeostasis and inflammation; and tissue damage occurs. Focusing attention on this interaction and its breakdown may allow a better understanding of the CD pathogenesis and lead to novel translational avenues for preventing and treating this widespread disease.
Highlights
Celiac disease (CD) is an immune-based enteropathy triggered by dietary wheat gluten and similar proteins in barley and rye in genetically susceptible individuals
CD is a T-cell mediated disease, in which gliadin-derived peptides activate lamina propria infiltrating T lymphocytes [2]. These latter represent the pivotal cells that orchestrate tissue damage. This leads to the release of proinflammatory cytokines, such as IFN-γ and IL-15 [3] which are responsible for the activation of the cytotoxic activity of intraepithelial lymphocytes (IELs) that leads to a profound tissue remodeling [4]
Even though changes of the microbiota could be linked to the etiopathogenesis of these diseases, further studies are needed to understand how to modulate microbiota to ameliorate the morbidity of CD
Summary
Celiac disease (CD) is an immune-based enteropathy triggered by dietary wheat gluten and similar proteins in barley and rye in genetically susceptible individuals. CD is a T-cell mediated disease, in which gliadin-derived peptides activate lamina propria infiltrating T lymphocytes [2] These latter represent the pivotal cells that orchestrate tissue damage. This leads to the release of proinflammatory cytokines, such as IFN-γ and IL-15 [3] which are responsible for the activation of the cytotoxic activity of intraepithelial lymphocytes (IELs) that leads to a profound tissue remodeling [4]. This is a complex disorder, with environmental and immune-genetic factors contributing to its etiology. Genetic, and environmental factors must be involved in CD onset [7]
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