Abstract
Celiac disease (CD) is an autoimmune enteropathy that occurs in genetically susceptible individuals exposed to dietary gluten. CD occurs in approximately 1 in 133 persons in the United States [1], although most are undiagnosed. Young children with CD present with diarrhea and malabsorption, but CD is also associated with extraintestinal autoimmune disorders, infertility, miscarriages, and cancer [2]. Ingestion of gluten is the most important environmental factor that correlates with CD [3]. Accordingly, current treatment strategies are centered on maintaining a gluten-free diet, which is challenging for many with CD [4]. Because of the increasing prevalence of CD [5] and the consequences of misdiagnosis, it is essential to better understand CD pathogenesis.
Highlights
Celiac disease (CD) is an autoimmune enteropathy that occurs in genetically susceptible individuals exposed to dietary gluten
Despite anecdotal and clinical implications that microbial pathogens act as triggers of CD, little is known about the mechanisms by which infectious agents evoke the disease
Oral tolerance prevents delayed-type hypersensitivity (DTH) responses by inhibiting T-cell proliferation, cytokine production, and serum antibodies against the food protein [12, 13]
Summary
Celiac disease (CD) is an autoimmune enteropathy that occurs in genetically susceptible individuals exposed to dietary gluten. CD occurs in approximately 1 in 133 persons in the United States [1], most are undiagnosed. Young children with CD present with diarrhea and malabsorption, but CD is associated with extraintestinal autoimmune disorders, infertility, miscarriages, and cancer [2]. Ingestion of gluten is the most important environmental factor that correlates with CD [3]. Current treatment strategies are centered on maintaining a gluten-free diet, which is challenging for many with CD [4]. Because of the increasing prevalence of CD [5] and the consequences of misdiagnosis, it is essential to better understand CD pathogenesis
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