Editing Sjögren's disease (section)

=== 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]].<ref name="pmid12524386">{{cite journal | vauthors = Takeda K, Kaisho T, Akira S | title = Toll-like receptors | journal = Annu. Rev. Immunol. | volume = 21 | pages = 335–76 | date = 2003 | pmid = 12524386 | doi = 10.1146/annurev.immunol.21.120601.141126 }}</ref> Although several infectious, [[exogenous]] agents have been implicated in the pathogenesis of Sjögren's disease, such as [[Epstein-Barr virus]] (EBV), [[human T-lymphotropic virus 1]], and [[hepatitis C virus]], their association with Sjögren's disease 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 the inability of lymphoid infiltrates to control EBV [[Viral replication|replication]] in Sjögren's disease, leading to the [[Initiation (chemistry)|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 disease, and which specific molecular mechanisms are involved in the process of viral reactivation,  remain to be clarified.<ref name="pmid8391219">{{cite journal | vauthors = Pflugfelder SC, Crouse CA, Monroy D, Yen M, Rowe M, Atherton SS | title = Epstein-Barr virus and the lacrimal gland pathology of Sjögren's syndrome | journal = Am. J. Pathol. | volume = 143 | issue = 1 | pages = 49–64 | date = July 1993 | pmid = 8391219 | pmc = 1886957 }}</ref>