Abstract
Progress in celiac disease (CD) research has been spectacular in recent years. The nature of gluten-derived peptides that are recognized by gut-derived T cells from patients, and that are therefore likely to be involved in disease development, has been elucidated (1–5). It has further been established that a ubiquitous enzyme modifies such peptides, leading to improved binding of such peptides to HLA-DQ2/8 molecules (6, 7). This now establishes a molecular basis for the well-known association between CD and the expression of these HLA-DQ molecules (8, 9). CD is therefore the best-characterized HLA-associated disease to date. However, several issues remain unclear. Why does the disease develop in only a small percentage of the individuals who carry the predisposing HLA-DQ molecules? Why does this disease severely affect some patients while others have only mild or no clinical symptoms? Can we use our current knowledge to prevent or cure this disease?
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