Abstract
Aim The aim of this study was to evaluate the expression of persistence of mumps virus and some cells that interact with viral infection in the focus of the autoimmune epithelitis and peripheral blood of Sjögren's syndrome patients in comparison to patients with rheumatoid arthritis (RA) and nonautoimmune sicca syndrome (nSS). Materials and Methods 126 patients (119 women and 7 men) were grouped into four groups: (1) patients with primary Sjögren's syndrome (pSS), (2) patients with secondary Sjögren's syndrome due to rheumatoid arthritis (sSS), (3) patients with rheumatoid arthritis (RA), and (4) patients with nonautoimmune sicca syndrome (nSS). Immunohistochemical analysis of immune response to the suggested silent persistence of mumps virus in the minor labial salivary gland biopsies and flow cytometric analysis of blood cells was done. Results Immunohistochemical signs of mumps virus persistence were found in the minor salivary glands of all study groups. Also, a significantly different immune response to virus infection (protein IFI16, interferons gamma and beta, dendritic cells, and receptor for natural killers) was revealed in the minor salivary glands of the study groups. Cytometric analysis of the blood cells revealed a dropping amount of circulating natural killers and dendritic cells in patients with SS. Significant correlations between immunohistochemical staining and serological findings were revealed. Conclusions Abundant immunohistochemical signs of mumps virus protein in the salivary glands and depletion of circulating immune cells make a background for thought of presumable mumps or/and other virus participation in epithelial damage causing sicca syndrome in predisposed patients.
Highlights
Sjögren’s syndrome is a common autoimmune disease characterised by sicca symptoms and extraglandular features
Patients enrolled in the study were recruited from the Rheumatology Center of Vilnius University Hospital Santara Clinics. 126 patients (119 women and 7 men) were grouped into four: (1) patients with primary Sjögren’s syndrome, (2) patients with secondary Sjögren’s syndrome due to rheumatoid arthritis, (3) patients with rheumatoid arthritis (RA), and (4) patients with nonautoimmune sicca syndrome
Analysis of the salivary gland tissue showed histopathological heterogeneity amongst s syndrome (SS) patients, including an extent of the cellular inflammatory infiltrate and the degree of epithelial damage in acini and ducts, healing either replacement of parenchymal glandular tissue by fat or fibrosis. primary Sjögren’s syndrome (pSS) sialadenitis revealed a focal proliferation of ductal epithelial cells combined with focal lymphocytic infiltration and atrophy of acini
Summary
Sjögren’s syndrome is a common autoimmune disease characterised by sicca symptoms and extraglandular features. Etiology and detailed pathogenesis of Sjögren’s syndrome (SS) are obscure [1]. Both innate and adaptive immune responses are implicated in the causation of SS, possibly triggered by viral infections and hormonal factors in a genetically susceptible host [2, 3]. The environmental triggers are believed to be infectious agents, which are most likely a virus [4, 5]. The wide spectrum of glandular and extraglandular manifestations in Sjögren’s syndrome raises a hypothesis about the cooperation of infections agents in the mechanisms of this disease.
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