Primary Sjögren’s syndrome (pSS) is a connective tissue disease characterized by a wide spectrum of clinical features, extending from a benign glandular disease to an aggressive systemic disorder and/or lymphoma. The pathogenesis of Sjögren’s syndrome (SS) is not completely understood, but it is assumed that pathogenesis of SS is multifactorial. The studies based on the animal models of SS provided significant insight in SS disease pathogenesis and management. The aim of this review is to summarize current studies on animal models with primary SS-like symptoms and discuss the impact of these studies on better understanding pathogenesis and management of Sjögren’s syndrome. Databases PubMed, Web of Science, Scopus and Cochrane library were searched for summarizing studies on animal models in SS. Available data demonstrate that animal models are highly important for our understanding of SS disease.

Primary Sjögren’s syndrome (pSS) is a heterogeneous chronic autoimmune disorder with multiple clinical manifestations that can develop into non-Hodgkin’s lymphoma in mucosa-associated lymphoid tissue. The pathogenesis of Sjögren’s syndrome (SS) is not completely understood, but it is assumed that pathogenesis of SS is multifactorial. The microbiota plays a notable role in the development of autoimmune disorders, including Sjögren’s syndrome. Molecular mimicry, metabolite changes and epithelial tolerance breakdown are pathways that might help to clarify the potential contribution of the microbiota to SS pathogenesis. This review aims to provide an overview of recent studies describing microbiota changes and microbiota mechanisms associated with Sjögren’s syndrome. Data on the microbiota in SS from PubMed, Web of Science, Scopus and the Cochrane Library databases are summarized. Overall, the microbiota makes a major contribution to the development of Sjögren’s syndrome and progression. Future microbiota studies should improve the management of this heterogeneous autoimmune disease.

Objectives: This study aims to investigate the distribution of myeloid-derived suppressor cells (MDSCs) in patients with primary or secondary Sjögren’s syndrome (SS) or rheumatoid arthritis (RA) in order to better understand MDSCs significance in the pathogenesis of these autoimmune diseases. Patients and methods: We examined the frequency and calculated absolute counts of overall MDSCs (human leukocyte antigen-antigen D related (HLA-DR)low/cluster of differentiation (CD) 33+/CD11b+) and monocytic MDSCs (HLA-DRlow/CD33+/CD11b+/CD14+) subset in peripheral blood samples of 23 RA (5 males, 18 females; mean age 57 years; range 41 to 81 years), 25 primary Sjögren’s syndrome (pSS) (1 male, 24 females; mean age 56 years; range 32 to 77 years), 17 secondary Sjögren’s syndrome (sSS) (1 male, 16 females; mean age 60 years; range 49 to 73 years) and 23 nonautoimmune sicca syndrome (nSS) (23 females; mean age 59 years; range 44 to 92 years) patients by flow cytometric analysis. Results: Analysis revealed that the frequency of overall MDSCs increased in RA group (46.5±3.4) compared with nSS group (35.6±3.2; p=0.0322). An increase of absolute count of overall MDSCs was most evident in both RA (4383±456.8) and sSS groups (3890±495.7) compared with pSS (2447±275.1; p=0.0002 and 0.0067) and nSS groups (2025±218.1; p

Background and Objectives: Systemic small-vessel vasculitis (SV) represents a group of rare autoimmune disorders with varied etiologies and clinical manifestations. Audiovestibular involvement in SV may present with a broad spectrum of symptoms, often complicating diagnosis and management. This study aimed to evaluate auditory function and speech perception in individuals diagnosed with SV and to investigate associations with disease-specific clinical parameters. Materials and Methods: A total of 40 patients diagnosed with SV (mean age: 48.9 years; range: 28–65 years) were recruited for comprehensive audiological assessment. The evaluation protocol included otoscopic examination, tympanometry, pure-tone audiometry, and speech audiometry. Statistical analysis was conducted using R software (version 4.3.1), and significance was set at p < 0.05. Results: Diagnoses included granulomatosis with polyangiitis (52.5%), eosinophilic granulomatosis with polyangiitis (27.5%), necrotizing vasculopathy (12.5%), and microscopic polyangiitis (7.5%). Mean disease duration was 4.14 years. Hearing complaints were reported by 77.5%; in 20%, they were the initial symptoms. Audiometry identified hearing loss in 50% of patients—predominantly sensorineural (33.8%), followed by mixed (13.7%) and conductive (2.5%) types. Hearing loss was most frequent in necrotizing vasculopathy (60%) and among ANCA-positive individuals (53.7%). Conclusions: Sensorineural hearing loss is common in SV, particularly in ANCA-positive patients, highlighting the need for routine hearing assessment in SV management.

Sjögren’s disease (SjD), or primary Sjögren’s syndrome (pSS), is a heterogeneous chronic autoimmune disorder with multiple clinical manifestations that can develop into non-Hodgkin’s lymphoma in mucosa-associated lymphoid tissue. SjD is one of the autoimmune diseases with the maximum delayed diagnosis due to its insidious onset, heterogeneous clinical features and varied course. It is increasingly recognized that extraglandular manifestations represent a clinical challenge for patients with SjD. The European League Against Rheumatism (EULAR) Sjögren’s Syndrome (SS) Disease Activity Index (ESSDAI) is a systemic disease activity index designed to measure disease activity in patients with primary Sjogren’s syndrome. It consists of 12 domains: cutaneous, pulmonary, renal, articular, muscular, peripheral nervous system, central nervous system, hematological, glandular, constitutional, lymphadenopathy and lymphoma, biological. More than a quarter of patients with pSS may have systemic features that are not included in the ESSDAI classification, i.e., various cardiovascular, ophthalmic, ENT, and other systemic or organ involvement that increase the magnitude of the systemic phenotype in the disease. The ESSDAI also excludes the gastrointestinal (GI) tract, and unfortunately, GI manifestations are not routinely assessed. Gastroesophageal reflux disease (GERD) is one of the most prevalent gastrointestinal disorders, impairing quality of life and consuming a large volume of medical resources. Recently carried out the Mendelian randomized trial confirmed the causal link between SjD and gastroesophageal reflux disease (GERD) and showed that GERD is a risk factor for SjD. This review aims to provide an overview of the research describing evidenced based links between Sjögren’s disease and gastroesophageal reflux disease, with the intention of ensuring that any systemic pathology in Sjögren’s disease is properly assessed and that management of the disease is directed towards the patient. A comprehensive literature search was carried out on PubMed, Web of Science, Scopus and the Cochrane Library databases. Two researchers searched for published studies indexed from inception to 1 September 2024 using the keywords ‘Sjögren’s syndrome’ OR ‘Sjögren’s disease’ AND ‘gastroesophageal reflux disease’ AND ‘microbiota’ OR microbiota dysbiosis’. We limited our search for scientific articles to human studies, and only included articles in English. Overall, there is a lack of evidence-based studies assessing the association between GERD and Sjögren’s disease and the changes in the microbiota associated with GERD in a multidisciplinary setting. Such studies are needed for the future, as this will improve the early diagnosis of Sjögren’s disease and the personalized management of the disease.

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.