Celiac Disease: Lessons for and from Chemical Biology.
Celiac disease is a lifelong immune disorder of the small intestine where inflammation is triggered by dietary gluten. There is an urgent need for the development of nondietary therapies for this widespread but overlooked disease. More fundamentally, a molecular understanding of gluten-induced pathogenesis in celiac disease has the potential to provide new insights into mucosal immunology. Over the past two decades, three pathogenically critical molecules-gluten, TG2, and HLA-DQ2-have served as focal points for collaborative efforts between biologists, chemists, engineers, and clinicians with an interest in celiac disease. This perspective summarizes a few examples of such multidisciplinary research directions with an emphasis on groundbreaking clinical studies that have profoundly informed the trajectory of subsequent molecular investigations. Examples of future challenges in fundamental and translational celiac disease research are also discussed.
Stanford ChEM-H & Departments of Chemistry and Chemical Engineering, Stanford University , Stanford, California 94305, United States.
Chaitan
0000-0001-6529-495X
C
Khosla
D001669:Biochemical Phenomena; D002446:Celiac Disease / Q000628:therapy*; D019204:GTP-Binding Proteins; D005983:Glutens; D006683:HLA-DQ Antigens; D006302:Health Services Research / Q000639:trends; D006801:Humans; D000091345:Protein Glutamine gamma Glutamyltransferase 2; D011503:Transglutaminases
D006683:HLA-DQ Antigens; C053186:HLA-DQ2 antigen; D005983:Glutens; D000091345:Protein Glutamine gamma Glutamyltransferase 2; D011503:Transglutaminases; D019204:GTP-Binding Proteins