Abstract
Celiac is a chronic enteric disease resulted from an abnormal immune response to gluten proteins in patients having a certain genomic constitution. Tissue transglutaminase enzyme 2 converts the glutamine residues of gluten peptides by deamidation reaction into glutamic acid, which binds to human leukocyte antigen (HLA)-DQ2 or -DQ8 molecules and subsequently evokes T cell responses leading to small intestine inflammation. These events lead to the typical symptoms associated with celiac disease. Also, wheat proteins are rich in proline content and are resistant to human pancreatic and gastric enzymes. Different peptidases from microbial and fungal sources can degrade these incompletely digested peptides. While following a gluten-free diet is the best preventive strategy, a combination therapy by using proteases or carboxypeptidases from microbial sources for gluten detoxification or treatment with tissue transglutaminase inhibitors may also be a good option. Intestinal epithelial cell lines (Caco-2) may be used as in vitro model to study trans/paracellular permeability, distortion of intercellular tight junction protein viz., occludin, and ZO-1, and rearrangement of actin filaments.
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Mukhopadhyay, C.D. (2022). Current Advances in Celiac Disease: Consequences and Improvement Strategies. In: Singh Deora, N., Deswal, A., Dwivedi, M. (eds) Challenges and Potential Solutions in Gluten Free Product Development. Food Engineering Series. Springer, Cham. https://doi.org/10.1007/978-3-030-88697-4_1
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