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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?

Interplay between genetics and the environment in the development of celiac disease: perspectives for a healthy life