Current opinion in rheumatology · 2016
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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Nakamura Hideki, Kawakami Atsushi
Аннотация
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.
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.