The only current treatment for celiac disease, a disorder of the small intestine that results from a hypersensitivity to ingested gluten, is lifelong adherence to a gluten-free diet. However, it is difficult to follow such a diet, and any slipups can result in damage to the small intestine. A paper published in Nature Genetics identifies genetic variation in eight different regions of the genome that could contribute to celiac disease pathophysiology.1 The finding potentially opens up multiple avenues for developing compounds that target the genetic or biochemical events underlying the disease.
The majority of celiac patients have variations in the HLA-DQ gene, which codes for major histocompatibility complex class II DQ,
a cell-surface receptor on antigen-presenting cells. The variants