Abstract
Viruses are possible pathogenic agents in several autoimmune diseases. Sjögren’s syndrome (SS), which involves exocrine dysfunction and the appearance of autoantibodies, shows salivary gland- and lacrimal gland-oriented clinical features. Epstein-Barr virus (EBV) is the most investigated pathogen as a candidate that directly induces the phenotype found in SS. The reactivation of the virus with various stimuli induced a dysregulated form of EBV that has the potential to infect SS-specific B cells and plasma cells that are closely associated with the function of an ectopic lymphoid structure that contains a germinal center (GC) in the salivary glands of individuals with SS. The involvement of human T-cell leukemia virus type 1 (HTLV-1) in SS has been epidemiologically established, but the disease concept of HTLV-1-associated SS remains unexplained due to limited evidence from basic research. Unlike the cell-to-cell contact between lymphocytes, biofilm-like structures are candidates as the mode of HTLV-1 infection of salivary gland epithelial cells (SGECs). HTLV-1 can infect SGECs with enhanced levels of inflammatory cytokines and chemokines that are secreted from SGECs. Regardless of the different targets that viruses have with respect to affinitive lymphocytes, viruses are involved in the formation of pathological alterations with immunological modifications in SS.
Highlights
The pathogenesis of Sjögren’s syndrome (SS), which affects salivary glands (SGs) as well as lacrimal glands (LGs), involves multiple factors including genetic elements [1,2,3] and subsequent environmental factors [4]
With regard to human T-cell leukemia virus type 1 (HTLV-1) genes other than the previously reported genes, we examined the expressions of HTLV-1 bZIP factor (HBZ) and tax gene by in situ hybridization (ISH), which showed that both genes expressed in infiltrating mononuclear cells (MNCs) and salivary gland epithelial cells (SGECs) from HTLV-1-associated myelopathy (HAM)-SS patients and a patient with adult T-cell leukemia (ATL), the expression of tax gene was dominant in MNCs of the HAM-SS patients [127] (Figure 1A,B)
With regard to HTLV-1 genes other than the previously reported genes, we examined the expressions of HTLV-1 bZIP factor (HBZ) and tax gene by ISH, which showed that both genes expressed in infiltrating MNCs and SGECs from HAM-SS patients aJ.nCdlina
Summary
The pathogenesis of Sjögren’s syndrome (SS), which affects salivary glands (SGs) as well as lacrimal glands (LGs), involves multiple factors including genetic elements [1,2,3] and subsequent environmental factors [4]. Viral infections are profoundly associated with the activation of innate immunity, followed by an acquired immune response. With the activation of an innate immunity signal with an interferon-gamma (IFN-γ) signature in viruses, the subsequent function of antigen presentation through the induction of major histocompatibility complex (MHC) is followed by an expansion of antigen-specific autoreactive T cells. We focus on the actions of Epstein-Barr virus (EBV) and retroviruses by comparing the effects of these viruses in salivary glands of individuals with Sjögren’s syndrome, as well as on the epidemiological and immunological findings
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