Sjögren's syndrome is an autoimmune disease characterized by dysfunction and inflammation of the salivary and lacrimal glands
The pathogenesis of Sjögren's syndrome has not been elucidated, but the role of viruses has been suggested.
Ebv-miR-BART13-3p downregulates STIM1 affecting the calcium influx mechanisms that regulate salivary gland function.
In this study we report that the EBV-specific microRNA ebv-miR-BART13-3p, that is significantly elevated in salivary glands of primary Sjögren's syndrome patients, targets stromal interacting molecule 1 (STIM1), a primary regulator of the store-operated Ca2 + entry pathway that is essential for salivary gland function. This interaction affects the intracellular Ca2 + entry and subsequently the Ca2 +-dependent activation of NFAT. Ebv-miR-BART13-3p is present in both B cells and salivary epithelial cells, even though EBV infects B cells and not salivary epithelial cells.
We demonstrate here that ebv-miR-BART13-3p can be transferred from B cells to salivary epithelial cells through exosomes, recapitulating the functional effects on calcium signaling.