Celiac disease (CeD) is a gluten-induced enteropathy that develops in genetically susceptible individuals on consumption of cereal gluten proteins. It is a unique complex immune disorder to study as the driving antigen is known and the tissue targeted by the immune reaction can be interrogated. This review integrates findings gained from genetic, biochemical and immunological studies, which together have revealed mechanisms of gluten peptide modification and HLA binding thereby enabling a maladapted anti-gluten immune response.
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