In genetically predisposed individuals, dietary
gluten in wheat, rye and barley triggers
celiac disease, a systemic autoimmune disorder hallmarked by an extensive small-bowel mucosal immune response. The current conception of
celiac disease pathogenesis is that it involves components of both innate and adaptive immunity whose activation typically leads to small-bowel villous
atrophy with crypt
hyperplasia. Currently, the only effective treatment for
celiac disease is a strict lifelong
gluten-free diet excluding all wheat-, rye- and barley-containing food products. During the diet, the clinical symptoms improve and the small-bowel mucosal damage recovers, while re-introduction of
gluten into the diet leads to re-appearance of the symptoms and deterioration of the small-bowel mucosal architecture. In view of the restricted nature of the diet, alternative treatment is warranted. Improved understanding of the molecular basis of
celiac disease has enabled researchers to suggest other therapeutic approaches. Although there is no animal model reproducing all features of
celiac disease, the use of in vitro approaches including a variety of cell lines and the celiac patient small-bowel mucosal biopsy organ culture has generated knowledge about pathogenesis of
celiac disease. In these culture systems,
gluten induces different effects that can be quantified, thus also enabling studies concerning the efficacy of candidate therapeutic compounds for
celiac disease. This review describes the intestinal epithelial cell models, celiac patient T-cell lines and clones, as well as the small-bowel mucosal organ culture methods widely used in studies of
celiac disease, and summarizes the major findings obtained with these systems.