Abstract
Celiac disease (CeD) is an autoimmune condition driven by gluten in genetically predisposed individuals. CeD is characterized by small intestinal villous atrophy but presents with a spectrum of gastrointestinal and systemic manifestations. Its only treatment is a strict, life-long adherence to a gluten-free diet, which is difficult to manage and does not always lead to symptomatic or mucosal recovery. About 40% of the population express the CeD-associated risk genes, but only 1%-2% of the worldwide population has CeD. This, along with the rising prevalence of CeD suggests other cofactors in disease pathogenesis. The gut microbiome has been implicated in CeD based on epidemiology studies and clinical associations. Mechanistic studies using relevant in vitro and in vivo preclinical models have begun to elucidate mechanisms through which microbes can influence CeD. Ultimately, a better understanding of these cofactors and their mechanisms will provide rationale intervention strategies and novel therapeutic targets to prevent or treat CeD.