INFECTION AND AUTOIMMUNITY: Edited by Gary HoffmanWhat is the evidence for Sjögren's syndrome being triggered by viral infection? Subplot: infections that cause clinical features of Sjögren's syndromeNakamura, Hideki; Kawakami, AtsushiAuthor Information Unit of Translational Medicine, Department of Immunology and Rheumatology, Nagasaki University Graduate School of Biomedical Sciences, Nagasaki, Japan Correspondence to Hideki Nakamura, Unit of Translational Medicine, Department of Immunology and Rheumatology, Nagasaki University Graduate School of Biomedical Sciences, 1-7-1 Sakamoto, Nagasaki City, Nagasaki 852-8501, Japan. Tel: +81 95 819 7262; fax: +81 958 49 7270; e-mail: firstname.lastname@example.org Current Opinion in Rheumatology: July 2016 - Volume 28 - Issue 4 - p 390-397 doi: 10.1097/BOR.0000000000000287 Buy Metrics Abstract Purpose of review 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. Recent findings 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. Summary 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. Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved.