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Curr Opin Rheumatol. 2016 Jul;28(4):390-7. doi: 10.1097/BOR.0000000000000287.

What is the evidence for Sjögren's syndrome being triggered by viral infection? Subplot: infections that cause clinical features of Sjögren's syndrome.

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Unit of Translational Medicine, Department of Immunology and Rheumatology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan.



To clarify the involvement of viral infections in the pathogenesis of Sjögren's syndrome and to discuss whether viruses can be a trigger for the development of Sjögren's syndrome.


Although some viruses are candidate triggers of Sjögren's syndrome, we focus on human T lymphotropic virus type I (HTLV-I). Clinicoepidemiological studies show a relationship between HTLV-I and Sjögren's syndrome with a low frequency of salivary gland damage in magnetic resonance imaging, autoantibody production and ectopic germinal center in HTLV-I-associated myelopathy (HAM) patients with Sjögren's syndrome. Our recent study showed that HTLV-I has the potential to infect salivary gland epithelial cells (SGECs). After a coculture of HCT-5 (an HTLV-I-infected T-cell line derived from the cerebrospinal fluid) of an HAM patient and SGECs, we observed time-dependent increases in the levels of soluble intracellular adhesion molecule1, interferon gamma-induced protein 10 kDa and regulated on activation, normal T-cell expressed and secreted. In addition, SGECs themselves express these molecules along with the expression of HTLV-I proteins.


HTLV-I is involved in the pathogenesis of HTLV-I-seropositive patients with Sjögren's syndrome. By infecting CD4 T cells in vivo, HTLV-I induces specific clinicopathological conditions. In addition, HTLV-I-infected SGECs have the potential to augment the expression of molecules involved in cell adhesion, inflammation and migration.

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