Researchers have developed the first truly accurate mouse model of celiac disease. The animals have the same genetic and immune system characteristics as humans who develop celiac after eating gluten. This provides a vital research tool for developing and testing new treatments for the disease.

«Based on our understanding of the human disease, we were able to retro-engineer a mouse model of celiac disease,» said Bana Jabri, MD, PhD, Director of Research at the University of Chicago Medicine Celiac Disease Center and senior author of the new study, published this week in Nature. «It’s the first model where the mouse develops damage to the small intestine just by eating gluten, which can later reverse itself on a gluten-free diet.»

Celiac disease is an autoimmune disorder that affects an estimated 1% of people worldwide. It causes gastrointestinal symptoms and damage to the lining of the small intestine when someone eats gluten, a protein found in grains such as wheat, barley and rye.

There is no cure, and the only effective treatment is a gluten-free diet, which can be difficult to maintain. Even the most careful celiac patients can accidentally ingest gluten through unknown ingredients in processed food or cross-contamination from foods containing gluten that are prepared nearby or with the same cooking equipment.

Even while maintaining a strict gluten-free diet, 40% of celiac disease patients still show signs of inflammation and villous atrophy, or damage to the villi, the small, finger-like protrusions in the small intestine that help absorb nutrients. Therefore, treatments that can reverse or prevent the disease are greatly needed to improve quality of life for people with celiac.

A complex interplay of contributing factors

Scientists do not know the exact cause of celiac disease, but researchers have identified several genetic, immune system, and environmental components that work together to trigger the disease. People with celiac have one of two genetic variants, HLA-DQ2 and HLA-DQ8, that are part of a group of genes that help the immune system recognize foreign antigens and mount an immune response. However, possessing one these variants is not sufficient to develop the disease alone.

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Materials provided by University of Chicago. Original written by Matt Wood. Note: Content may be edited for style and length.