Celiac disease (CeD) is a serious autoimmune disorder where the ingestion of gluten—a protein found in wheat, barley, and rye—triggers an immune response in the small intestine. This reaction can cause damage to the lining of the small intestine, leading to malabsorption of nutrients and a range of severe health complications. Globally CeD affects approximately 1.4% of the population and an estimated 3.3 million people in the USA alone, as indicated by seroprevalence studies. About 130,000 patients in the USA suffer from severe and refractory celiac disease, leading to additional complications such as malabsorption, ulcerative jejunitis, and enteropathy-associated T-cell lymphoma. Additionally, CeD patients miss about 50% more workdays compared to those without the disease, and they often face substantial psychosocial challenges. Celiac disease is strongly associated with specific HLA class II gene variants, particularly HLA-DQ2 and HLA-DQ8. Furthermore, CeD patients are 3-12 times more likely to develop non-Hodgkin’s lymphoma, a life-threatening complication. Management of the disease currently relies solely on a strict gluten-free diet, yet approximately 30% of patients continue to experience severe symptoms.