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Celiac disease (CD) is the most common autoimmune enteropathy, triggered by a deregulated immune response to gliadin. It has been hypothesized that human intestinal microbiota may interfere with the pathogenesis of the disease and in the clinical course of CD. In the present review, we analyzed the microbiota alterations observed in the course of CD, how they may influence the pathogenesis of CD, and the possible applications for a microbiota modulation in CD. In detail, most of the current literature underlined that the dysbiosis in CD is hallmarked by an increase in gram-negative and Bacteroidetes species, and by a decrease in Bifidobacteria and Lactobacilli. As the intestinal microbiota is able to modulate the cytokine environment, an unfavorable microbiota could amplify the immune response to gliadin in individuals with CD, whereas the administration of probiotic species could lead to a decrease in proinflammatory cytokine production. Therefore, dysbiosis could represent an important trigger in CD pathogenesis, along with genetic (HLA—haplotypes) and environmental factors (antibiotic administration, mode of delivery, and breastfeeding). Although data on the modulation of microbiota by GFD are conflicting, current evidence has demonstrated that probiotic administration could be useful to improve symptoms and to reduce molecular mucosal inflammation, by downregulating the cytokines involved in CD pathogenesis. However, studies analyzing this aspect are few in number, thus stimulating the exploration of this field, with the aim of achieving a solid pathophysiological basis for probiotic administration in CD.