The understanding of the pathogenesis of celiac disease has made huge advances in
recent years. The disease is caused by an inappropriate immune response to dietary gluten
proteins. This immune response is controlled by CD4+ T cells in the lamina propria that
recognize gluten peptides in the context of disease predisposing HLA-DQ2 and HLA-DQ8
molecules. 1, 2 These T cells are specific for proline-and glutamine-rich gluten peptides that
are resistant to proteolysis and that have been become deamidated by the enzyme …