シェーグレン症候群
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 Sjögren's syndrome, such as Epstein-Barr virus (EBV), human T-lymphotropic virus 1, and hepatitis C virus, their association with Sjögren's syndrome appears weak. While EBV is present in the salivary glands of normal individuals, a high incidence of EBV reactivation in Sjögren's patients has been reported with increased levels of EBV DNA. This indicates viral reactivation and inability of lymphoid infiltrates to control EBV replication in Sjögren's 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 Sjögren's syndrome, and which specific molecular mechanisms are involved in the process of viral reactivation, remain to be clarified.