Abstract
Celiac disease (CD) is an autoimmune and multisystem gluten-related disorder that causes symptoms involving the gastrointestinal tract and other organs. Pathogenesis of CD is only partially known. It had been established that ingestion of gluten proteins present in wheat and other cereals are necessary for the disease and develops in individuals genetically predisposed carrying the DQ2 or DQ8 human leukocyte antigen haplotypes. In this review, we had pay specific attention on the last discoveries regarding the three cellular components mainly involved in the development and maintenance of CD: T-cells, B-cells, and microbioma. All of them had been showed critical for the interaction between inflammatory immune response and gluten peptides. Although the mechanisms of interaction among overall these components are not yet fully understood, recent proteomics and molecular studies had shed some lights in the pathogenic role of tissue transglutaminase 2 in CD and in the alteration of the intestinal barrier function induced by host microbiota.
Highlights
Celiac disease (CD) is characterized by small intestinal mucosal injury and nutrient malabsorption [1]
Studies of stored serum showed an increase in CD prevalence from fourfold to fivefold over the past 50 years [2]
The geographic epidemiological distribution of CD along a north–south and west–east gradient in Europe related to socioeconomic status and observations from population migration suggests an environmental impact driving the increased incidence of CD but this topic is still more debated [3, 4]
Summary
Celiac disease (CD) is characterized by small intestinal mucosal injury and nutrient malabsorption [1]. Studies of stored serum showed an increase in CD prevalence from fourfold to fivefold over the past 50 years [2]. The geographic epidemiological distribution of CD along a north–south and west–east gradient in Europe related to socioeconomic status and observations from population migration suggests an environmental impact driving the increased incidence of CD but this topic is still more debated [3, 4]. Celiac disease clinical identification is based on histological evaluation of the small intestine biopsies. Serologic assays, such as immunoglobulin (Ig)-A tissue transglutaminase and endomysial antibody (EMA; IgA), may be useful to support the diagnosis [6]
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