Publications by authors named "Efstathia K Kapsogeorgou"

Primary Sjögren's syndrome (pSS) is a chronic autoimmune disorder with diverse clinical picture and high prevalence of B-cell non-Hodgkin lymphoma (NHL), that possibly raises from the chronic activation of B-cells. The mechanisms underlying the development of neoplasia in pSS remain elusive. Activated Akt/mTOR pathway is a uniform finding in cancer, whereas its significance in haematologic malignancies is highlighted by the plethora of inhibitors with promising therapeutic efficacy.

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Objectives: To assess the prevalence of autoantibodies (AAbs) in mechanically ventilated COVID-19 patients and to investigate whether AAbs influence the clinical outcome.

Methods: Serum samples were drawn within the first 48 hours upon admission to the intensive care unit (ICU) from 217 consecutive patients, from January 1st, 2021, to May 10th, 2021, and investigated for the presence of AAbs using conventional techniques. Serum samples (n=117) of age- and sex-matched healthy individuals collected before COVID-19 pandemic were used as controls.

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Primary Sjögren's syndrome (pSS) is an autoimmune exocrinopathy of mainly the salivary and lacrimal glands associated with high prevalence of lymphoma. Akt is a phosphoinositide-dependent serine/threonine kinase, controlling numerous pathological processes, including oncogenesis and autoimmunity. Herein, we sought to examine its implication in pSS pathogenesis and related lymphomagenesis.

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Recent studies suggest that elevated CXCL13 serum levels in patients with primary Sjögren's syndrome (pSS) associate with minor salivary gland (MSG) histologic features, disease severity, as well as high-risk status for non-Hodgkin lymphoma (NHL) development and NHL itself. In contrast, limited discriminative value of CXCL13 saliva levels has been reported. Prompt by these reports, we sought to validate the clinical utility of CXCL13 by investigating potential correlations of serum and saliva levels with MSG histopathologic [including CXCL13+-cell number, severity of infiltrates and germinal center (GC) formation], serologic and clinical parameters, as well as NHL.

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Sjögren's syndrome (SS) is a relatively common systemic autoimmune disease of unknown aetiology, although genetic, hormonal, immunologic, and environmental factors are thought to be involved in disease pathogenesis. It is also termed "autoimmune epithelitis", and afflicts mainly the epithelial structures of salivary and lachrymal glands, through periepithelial lymphocytic infiltration responsible for the occurrence of dryness symptoms. Sjögren's syndrome (SS) is also characterised by B cell hyperactivity as reflected by the presence of hypergammaglobulinemia and the production of autoantibodies, which seems to be associated with the presence of ectopic germinal centres within the inflamed minor salivary glands.

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The hematopoietic system relies on regulation of both metabolism and autophagy to maintain its homeostasis, ensuring the self-renewal and multipotent differentiation potential of hematopoietic stem cells (HSCs). HSCs display a distinct metabolic profile from that of their differentiated progeny, while metabolic rewiring from glycolysis to oxidative phosphorylation (OXPHOS) has been shown to be crucial for effective hematopoietic differentiation. Autophagy-mediated regulation of metabolism modulates the distinct characteristics of quiescent and differentiating hematopoietic cells.

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Perinuclear anti-neutrophilic cytoplasmic antibodies (P-ANCA) recognize heterogeneous antigens, including myeloperoxidase (MPO), lactoferrin, elastase, cathepsin-G and bactericidal/permeability-increasing protein. Although P-ANCA have diagnostic utility in vasculitides, they may also be found in patients with various other systemic autoimmune rheumatic diseases (SARDs). Nevertheless, the clinical significance and the targets recognized by P-ANCA in such patients remain unclear.

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Objectives: To explore the presence of neutrophil extracellular traps (NETs) in inflamed temporal artery biopsies (TABs) of patients with GCA.

Methods: Ten patients with GCA [five with limited and five with associated generalized vascular involvement, as defined by 18F-fluorodeoxyglucose PET with CT (PET/CT)] and eight with PMR were studied. The presence, location, quantitation and decoration of NETs with IL-6, IL-1β and IL-17A were assessed in TABs at the time of disease diagnosis by tissue immunofluorescence and confocal microscopy.

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Article Synopsis
  • This study looks at how a score from labial minor salivary glands (LMSG) can help find out if Sjögren's Syndrome (SS) patients might develop lymphoma, a type of cancer.
  • They analyzed 1,997 SS patients, focusing on those with a score of 1 or higher and found that higher scores meant a shorter time from SS diagnosis to lymphoma diagnosis.
  • The results suggest that a follow-up check at certain times can help catch lymphoma earlier in patients with higher scores.
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Sjögren's syndrome (SS) is characterized by the aberrant activation of B-cells in both the target organs of autoimmune responses, such as the exocrine glands and the periphery. Furthermore, SS is strongly associated with the development of B-cell non-Hodgkin lymphomas, which are considered to result from chronic aberrant activation of B-cells. Disturbances of the minor salivary gland (MSG) infiltrating and peripheral B-cells subpopulations have been described in SS patients; however, the underlying mechanisms have not been uncovered.

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Sjögren's syndrome (SS) is a chronic systemic autoimmune disease, affecting predominantly the exocrine glands, a large array of systemic manifestations and high risk of lymphoma development. The latter constitutes the major adverse outcome of SS contributing in the increased morbidity and mortality of the disease. The vast majority of lymphomas in SS are B-cell non-Hodgkin's lymphomas (NHL), primarily indolent mucosa-associated lymphoid tissue (MALT) lymphomas, followed by nodal marginal zone lymphomas (NMZL) and diffuse large B cell lymphomas (DLBCL).

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The data presented here are related to the research article titled " (Vakrakou et al., Journal of Autoimmunity, in press, 2017). In the cited manuscript, using comparative analyses of salivary gland biopsy specimens and ductal salivary gland epithelial cell (SGEC) lines from SS patients and disease controls, we have demonstrated that the ductal epithelia of SS patients display constitutively reduced PPARγ expression, transcriptional activity and anti-inflammatory function that were associated with cell-autonomously activated NF-κB and IL-1β pathways in these cells.

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Objectives: Development of non-Hodgkin's lymphoma (NHL) is the major adverse outcome of Sjögren's syndrome (SS) affecting both morbidity and mortality. Preliminary evidence suggested that, although not deregulated compared with sicca controls, miR200b-5p levels are decreased in the minor salivary glands (MSGs) of SS patients with NHL. The aim of the current study was to evaluate the MSG expression of miR200b-5p in SS-associated NHLs and its potential predictive value for the identification of patients with SS susceptible to develop NHL.

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Background: Development of non-Hodgkin's lymphoma (NHL) is the major adverse outcome of primary Sjögren's Syndrome (pSS) affecting both morbidity and mortality. The high frequency of transformation to lymphoid malignancy in pSS among autoimmune rheumatic diseases (6-10% of patients) and the accessibility of the affected organ (minor salivary glands; MSG), render pSS an ideal model for the study of lymphomagenesis associated with autoimmune diseases and inflammation. Although pSS-related lymphoid transformation is generally considered as an antigen-driven, multi-step process owed to the chronic activation of B-cells in MSGs, the underlying mechanisms remain elusive.

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Sjögren's syndrome (SS) patients manifest inflammation in the salivary glands (SG) and evidence of persistent intrinsic activation of ductal SG epithelial cells (SGEC), demonstrable in non-neoplastic SGEC lines derived from patients (SS-SGEC). The peroxisome-proliferator-activated receptor-γ (PPARγ) mediates important anti-inflammatory activities in epithelial cells. Herein, the comparative analysis of SG biopsies and SGEC lines obtained from SS patients and controls had revealed constitutively reduced PPARγ expression, transcriptional activity and anti-inflammatory function in the ductal epithelia of SS patients that were associated with cell-autonomously activated NF-κB and IL-1β pathways.

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Autoimmune diseases constitute a diverse group of disorders characterized by cellular and humoral responses against self. The humoral autoimmune responses are directed against various cellular and extracellular components. These responses are highly specific for each autoimmune disease and result in the production of autoantibodies that characterize certain disease entities, representing a valuable tool for the diagnosis of autoimmune diseases.

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Sjögren's syndrome (SS) is a chronic autoimmune disease with broad clinical spectrum, extending from benign exocrinopathy to severe systemic disease and lymphoma development. The glandular and extraglandular dysfunction of SS is associated with lymphocytic infiltrates that invade the epithelial structures of affected organs. The in-depth study of autoimmune lesions in the minor salivary glands (MSG), which are the major target-organ of SS responses, revealed that the lymphocytic infiltrates vary in severity and composition among SS-patients, are full-blown at diagnosis and remain unchanged thereafter.

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Objectives: The aetiology of primary Sjögren's syndrome (pSS), also referred to as autoimmune epithelitis, is incompletely understood but includes an epigenetic contribution. Accordingly, the aim of this study was to investigate DNA methylation in salivary gland epithelial cells (SGEC), and to compare results with those publicly available from pSS B and T cells.

Methods: Long-term cultured SGEC were selected to conduct an epigenome-wide association study (EWAS) in patients with pSS with comparison to controls using the HumanMethylation 450 K array from Illumina.

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Objective: Increased expression of type I interferon (IFN) and a broad signature of type I IFN-induced gene transcripts are observed in patients with systemic lupus erythematosus (SLE) and other systemic autoimmune diseases. To identify disease-relevant triggers of the type I IFN pathway, this study sought to investigate whether endogenous virus-like genomic repeat elements, normally silent, are expressed in patients with systemic autoimmune disease, and whether these retroelements could activate an innate immune response and induce type I IFN.

Methods: Expression of type I IFN and long interspersed nuclear element 1 (LINE-1; L1) was studied by polymerase chain reaction, Western blotting, and immunohistochemistry in samples of kidney tissue from patients with lupus nephritis and minor salivary gland (MSG) tissue from patients with primary Sjögren's syndrome (SS).

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Both type I and II interferons (IFNs) have been implicated in the pathogenesis of Sjogren's syndrome (SS). We aimed to explore the contribution of type I and II IFN signatures in the generation of distinct SS clinical phenotypes including lymphoma development. Peripheral blood (PB) from SS patients (n = 31), SS patients complicated by lymphoma (n = 13) and healthy controls (HC, n = 30) were subjected to real-time PCR for 3 interferon inducible genes (IFIGs) preferentially induced by type I IFN, 2 IFIGs preferentially induced by IFNγ as well as for IFNα and IFNγ genes.

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Examination of biopsy-obtained salivary gland tissue provides valuable insights for the diagnosis, classification and treatment of patients with primary Sjögren syndrome. Could the study of biomarkers present in saliva provide a noninvasive alternative?

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Sjogren's syndrome (SS) has been associated with the expression of anti-Ro and anti-La antibodies. Anti-salivary gland protein 1 (SP1) antibodies have recently been identified in patients with SS. The current work involved a cross sectional study to determine whether anti-SP1 antibodies were identified in particular subgroups of patients with SS.

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Sjögren's syndrome (SS) is a systemic autoimmune disease characterized by periepithelial lymphocytic infiltrates in affected tissues and the production of plethora of autoantibodies. Among them autoimmune responses against Ro/SSA and La/SSB are of major importance since their detection is routinely used for disease diagnosis and clinical characterization. Although the exact mechanisms underlying disease pathogenesis are not fully understood, the important role of salivary gland epithelial cells (SGEC) in the initiation and development of the local immune responses is well-established.

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