Seropositivity for anti-Ro and anti-La is associated with greater severity and longer duration of disease, and findings of their high abundance from the salivary glands of Sjögrens patients suggests their imperative role in the pathogenesis of SS.Beyond genetics, epigenetic abnormality related to DNA methylation, histone acetylation, or microRNA expression probably has a key role in the pathogenesis of autoimmune diseases, including Sjögrens syndrome, though research in this area is very limited. Environmental triggers
Environmental factors, such as glandular viral infection, could prompt epithelial cells to activate the HLA-independent innate immune system through toll-like receptors. Although a number of infectious, exogenous agents have been implicated in the pathogenesis of Sjögrens syndrome, such as Epstein-Barr virus (EBV), human T-lymphotropic virus 1, and hepatitis C virus, their association with Sjögrens syndrome appears weak. While EBV is present in the salivary glands of normal individuals, a high incidence of EBV reactivation in Sjögrens patients has been reported with increased levels of EBV DNA. This indicates viral reactivation and inability of lymphoid infiltrates to control EBV replication in Sjögrens syndrome, leading to the initiation or perpetuation of an immune response in target organs. Nonetheless,  exactly how reactivation of EBV is induced in lesions of patients with Sjögrens syndrome, and which specific molecular mechanisms are involved in the process of viral reactivation,  remain to be clarified. Inflammation
Epithelial cells in Sjögrens syndrome lesions are active participants in the induction and perpetuation of the inflammatory process.
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