Abstract
Celiac disease (CD) is a systemic autoimmune disorder sustained by an inappropriate immune response to dietary gluten. We have provided experimental evidence that rotavirus infection may be involved in the pathogenesis of CD through a mechanism of molecular mimicry. In CD a subset of anti-transglutaminase IgA antibodies crossreact with the viral protein VP7. The same antibodies increase epithelial permeability upon interaction with desmoglein and activate innate immune responses upon engagment of TLR4. Moreover they modulate genes that are involved in apoptosis, inflammation, and alteration of the epithelial barrier integrity in intestinal epithelial cells, all typical features of CD. Noteworthy the anti-rotavirus VP7 antibodies are present in the patients’ sera before the CD onset, preceding the detection of anti-tTG and anti-endomysium antibodies.
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