Celiac disease (also known as celiac sprue) is a disorder of the digestive system, which occurs when the body reacts abnormally to gluten, a protein found in wheat, rye and barley. Consumption of gluten by celiac patients leads to the inflammation of the small intestine, tissue damage and in consequence decreased absorption of nutrients from food. Since the body's own immune system causes the damage, celiac disease is classified as an "autoimmune" disorder. Remarkably, celiac disease is associated with other autoimmune diseases such as type I diabetes, autoimmune thyroiditis or rheumatoid arthritis.

Celiac disease may be discovered at any age, from infancy through adulthood. So far over a hundred clinical manifestations of celiac disease have been described. Besides the typical consequences of malabsorption such as diarrhea and stomach ache, the symptoms may include anemia, fatigue growth arrest, infertility and osteoporosis.

The prevalence of celiac disease is about 1 per 100-200 people in the US and Europe. However, due to the common characteristics of the manifestations and low awareness of the medical community, celiac disease remains largely under-diagnosed.

The only treatment for celiac disease is a gluten-free diet. It may be easy for the doctor to prescribe, but difficult for the patient to follow. This is due to high abundance of gluten in popular foods as well as frequent contamination of products that usually should not contain gluten. Also, gluten-free products are usually much more expensive as they have to be stringently tested for the presence of gluten contaminants. Fortunately for most patients, adhering to the gluten-free diet readily alleviates the symptoms and facilitates recovery of the small intestine.

Research on celiac disease continues to be a challenge due to the lack of a reliable animal model. Still, certain aspects of the disease pathogenesis can be addressed using mice. Hilde Cheroutre, Ph.D., a world authority in intestinal immunology, is studying some early events in the pathogenesis of celiac disease. These studies aim at unraveling the role of intestinal infections in the gluten modification by enzyme tissue transglutaminase. Understanding the factors responsible for triggering the onset of celiac disease may facilitate development of the adequate mouse model. In addition, such knowledge may contribute to the development of protocols for prevention of the disease, as well as establishing treatment modalities seeking to reintroduce mucosal tolerance to gluten in celiac patients.