Celiac disease: mechanisms and emerging therapeutics.

Celiac disease (CeD) is a chronic inflammatory disorder that occurs in response to gluten-derived peptides in genetically susceptible individuals. The only currently approved treatment for CeD is life-long dietary exclusion of wheat and related cereal grains. The causative antigens, genetic background, and their interactions have been well characterized in CeD pathogenesis. Recent work has begun to elucidate additional genetic and environmental factors that are important for disease initiation and subsequent tissue damage. This molecular and cellular understanding of CeD pathogenesis has led to the development of numerous putative therapies that are currently being tested in the clinic. Celiac disease (CeD) is a widespread, gluten-induced, autoimmune disorder that lacks any medicinal therapy. Towards the goal of developing non-dietary treatments for CeD, research has focused on elucidating its molecular and cellular etiology. A model of pathogenesis has emerged centered on interactions between three molecular families: specific class II MHC proteins on antigen-presenting cells (APCs), deamidated gluten-derived peptides, and T cell receptors (TCRs) on inflammatory CD4+ T cells. Growing evidence suggests that this pathogenic axis can be pharmacologically targeted to protect patients from some of the adverse effects of dietary gluten. Further studies have revealed the existence of additional host and environmental contributors to disease initiation and tissue damage. This review summarizes our current understanding of CeD pathogenesis and how it is being harnessed for therapeutic design and development. [ABSTRACT FROM AUTHOR]