Search for: rheumatoid arthritis    methotrexate    autoimmune disease    biomarker    gene expression    GWAS    HLA genes    non-HLA genes   

ID PMID Title PublicationDate abstract
29347830 An OMIC biomarker detection algorithm TriVote and its application in methylomic biomarker 2018 Apr AIM: Transcriptomic and methylomic patterns represent two major OMIC data sources impacted by both inheritable genetic information and environmental factors, and have been widely used as disease diagnosis and prognosis biomarkers. MATERIALS & METHODS: Modern transcriptomic and methylomic profiling technologies detect the status of tens of thousands or even millions of probing residues in the human genome, and introduce a major computational challenge for the existing feature selection algorithms. This study proposes a three-step feature selection algorithm, TriVote, to detect a subset of transcriptomic or methylomic residues with highly accurate binary classification performance. RESULTS & CONCLUSION: TriVote outperforms both filter and wrapper feature selection algorithms with both higher classification accuracy and smaller feature number on 17 transcriptomes and two methylomes. Biological functions of the methylome biomarkers detected by TriVote were discussed for their disease associations. An easy-to-use Python package is also released to facilitate the further applications.
29387065 Heterogeneity of the Type I Interferon Signature in Rheumatoid Arthritis: A Potential Limi 2017 INTRODUCTION: An increased expression of interferon (IFN)-responding genes (IRGs), the so-called IFN signature, has been reported in rheumatoid arthritis (RA). However, some controversy exists concerning its clinical relevance. The main aim of this study is to evaluate whether quantitative and qualitative differences in the activation of the IFN pathway may account for these findings. METHODS: The expression of IFN-induced protein 44 (IFI44), IFN-induced protein 44 like (IFI44L), IFN alpha inducible protein 6, and MX dynamin-like GTPase 1 (MX1) was determined in peripheral blood in 98 RA patients (IFI6) and 28 controls. RA patients were classified into groups according to their clinical stage and treatments received: very early RA (VERA), biological disease-modifying antirheumatic drug (bDMARD) naive, and bDMARD. An additional group of 13 RA patients candidates for tumor necrosis factor alpha (TNFα) blockade was also recruited. The associations among IRGs were evaluated by network and principal component analyses. RESULTS: The expression of all IRGs was increased in RA to different levels. The IFN score was increased in all RA groups (VERA, bDMARD-naïve, and bDMARD), but important differences in their degree of activation and in the relationships among IRGs were observed. The IFN score correlated with the accumulated disease activity score 28-joints, and it was found to be a predictor of clinical outcome in VERA. No differences in the IFN score were observed between the bDMARD-naive and bDMARD groups, but opposite associations with the clinical parameters were noted. Interestingly, the correlations among IRGs delineate different pictures between these two groups. The IFN score at baseline predicted poor clinical outcome upon TNFα blockade. Although no absolute changes in the IFN score were found, TNFα-blockade shifted the associations among IRGs. CONCLUSION: A certain heterogeneity within the IFN signature can be recognized in RA, depending on the clinical stage. The structure of the IFN signature may be a potential explanation for the controversy in this field and must be considered to decipher its clinical relevancein RA.
30886977 Resveratrol displays anti-inflammatory properties in an ex vivo model of immune mediated i 2018 BACKGROUND: Resveratrol is a natural polyphenol found in berries, roots and wine that is well known to have anti-inflammatory and anti-oxidative properties. The anti-inflammatory effect has been reported for both immune cells and connective tissues, but only few studies have investigated effects on immune mediated inflammatory arthritis. None of which have studied this effect when combining resveratrol with methotrexate or adalimumab, two major drugs in the treatment of immune mediated inflammatory arthritis.We therefore aimed to investigate the anti-inflammatory effect of resveratrol alone and in combination with methotrexate or adalimumab in ex vivo models of immune mediated inflammatory arthritis. We furthermore aimed to describe any variations in this effect based on disease activity and cellular composition of the synovial fluid infiltrate. METHODS: Synovial fluid mononuclear cells from patients with rheumatoid arthritis (n = 7) and spondyloarthritis (n = 7) were cultured for either 48 h or 21 days. In both models, synovial fluid mononuclear cells were treated with resveratrol alone or in combination with methotrexate or adalimumab. Monocyte chemoattractant protein 1, matrix metalloproteinase 3 and tartrate resistant acidic phosphatase were measured to quantify inflammation, enzymatic degradation and osteoclast differentiation, respectively. RESULTS: Resveratrol reduced monocyte chemoattractant protein 1 production by synovial fluid mononuclear cells significantly (p = 0.005) compared to untreated controls. The effect of resveratrol was greatest in cultures from patients with low disease activity, i.e. DAS28CRP ≤ 3.2 (p = 0.022), and in cultures dominated by lymphocytes (p = 0.03). Further, the combination of methotrexate and resveratrol significantly reduced monocyte chemoattractant protein 1 levels compared with methotrexate alone in cultures from patients with low disease activity (p = 0.016), and in cultures with high lymphocyte count (p = 0.011). Resveratrol did not significantly affect matrix metalloproteinase 3 and tartrate resistant acidic phosphatase production. CONCLUSION: Resveratrol has anti-inflammatory properties in our ex vivo model of immune mediated inflammatory arthritis. Results show an additive effect of resveratrol, when combined with methotrexate in samples dominated by lymphocytes and samples from patients with low disease activity. This suggests further investigations in vitro and whether this effect may also be present in a clinical setting.
30513782 Sarcopenia in Patients with Rheumatic Diseases: Prevalence and Associated Risk Factors. 2018 Dec 1 The prevalence of sarcopenia in rheumatic diseases has been evaluated in single diseases using various diagnostic approaches, generating conflicting data on the pathogenetic mechanism(s). Herein, we evaluated both muscle mass index (MMI) and muscle strength to assess sarcopenia and presarcopenia in patients with rheumatoid arthritis (RA), psoriatic arthritis (PsA), and ankylosing spondylitis (AS). Moreover, we evaluated the possible impact of disease/patient-related characteristics, therapeutic regimens, and nutritional aspects on sarcopenia. The present study included 168 patients of both genders, aged 40⁻75 years. All patients underwent a nutritional evaluation, physical activity level assessment, rheumatologic evaluation, and an MMI and muscle strength assessment. The prevalence of sarcopenia was about 20% in all the three rheumatologic diseases, whereas presarcopenia was significantly different in RA, PsA and AS (p = 0.006). At multivariate analysis, only age ≥60 years and the presence of a disability were associated with a significantly increased risk of sarcopenia (p = 0.006 and p = 0.01, respectively), while a higher C-reactive protein did not reach statistical significance. Sarcopenia is similar in RA, PsA and AS, whereas presarcopenia significantly differs in these three diseases. Disease activity/inflammation and nutritional aspects do not influence sarcopenia, while age ≥60 years and the presence of a disability significantly increase the risk of sarcopenia.
28923440 Interstitial lung disease in the connective tissue diseases; a paradigm shift in diagnosis 2018 Jan Interstitial lung disease (ILD) in the connective tissue diseases (CTD) is amongst the most challenging aspect of care of patients with rheumatic diseases and is the source of significant morbidity and mortality. While there has been progress in our understanding of the natural history of these complications, we still suffer from a limited reservoir of data to confidently determine which patients are at highest risk for disease and those who are at highest risk for disease progression. Treatment options until recently have been limited to anti-inflammatory therapies but with the emerging availability of anti-fibrotic therapies, a shift in strategy is emerging to target therapies based on the specific radiographic, histopathologic features and biomarker profiles that are unique to patients with rheumatic diseases and ILD.
28913818 A Spectroscopic Study of Interaction of Auricyanide with n-Acetylcysteine. 2018 Jun Interaction of auricyanide, an important metabolite of anti-arthritic gold-based drug auranofin, was studied in vitro with a pharmacologically active ligand n-acetylcysteine with a view to understand reactivity of gold in vivo. Formation of reduction product aurocyanide occurred through mono- and di-n-acetylcysteine-substituted intermediates. The product and intermediates were identified and monitored spectrophotometrically and by electrospray ionization mass spectrometry. This study suggests successive substitution with n-acetylcysteine through trans effect. At equimolar concentrations of auricyanide and n-acetylcysteine, only mono-substituted mixed-ligand complex was formed. Substitution of the data obtained to various kinetic models suggested that the reaction orders are 0.6 in terms of n-acetylcysteine, 1.5 in terms of auricyanide, and 2 overall. The intermediates detected in this work may help to synthesize more effective and less toxic gold drugs.
31294239 Drug-microbiota interactions and treatment response: Relevance to rheumatoid arthritis. 2018 Knowledge about associations between changes in the structure and/or function of intestinal microbes (the microbiota) and the pathogenesis of various diseases is expanding. However, interactions between the intestinal microbiota and different pharmaceuticals and the impact of these on responses to treatment are less well studied. Several mechanisms are known by which drug-microbiota interactions can influence drug bioavailability, efficacy, and/or toxicity. This includes direct activation or inactivation of drugs by microbial enzymes which can enhance or reduce drug effectiveness. The extensive metabolic capabilities of the intestinal microbiota make it a hotspot for drug modification. However, drugs can also influence the microbiota profoundly and change the outcome of interactions with the host. Additionally, individual microbiota signatures are unique, leading to substantial variation in host responses to particular drugs. In this review, we describe several known and emerging examples of how drug-microbiota interactions influence the responses of patients to treatment for various diseases, including inflammatory bowel disease, type 2 diabetes and cancer. Focussing on rheumatoid arthritis (RA), a chronic inflammatory disease of the joints which has been linked with microbial dysbiosis, we propose mechanisms by which the intestinal microbiota may affect responses to treatment with methotrexate which are highly variable. Furthering our knowledge of this subject will eventually lead to the adoption of new treatment strategies incorporating microbiota signatures to predict or improve treatment outcomes.
30631629 Clinical Utility of Neutrophil CD64 to Detect Extrapulmonary Tuberculosis in Three Patient 2018 Biologics play a key role in the treatment of rheumatoid arthritis (RA), while RA-related serious infection remains an unsettled clinical problem. Detection of tuberculosis (TB) is challenging due to the difficulty in distinguishing symptoms such as fever and elevation of inflammatory markers from other infections or a disease flare of RA. The expression of the CD64 molecule on neutrophils (neutrophil CD64) was upregulated by various infections including TB. However, it was not affected by disease activity of RA or by any therapy against RA. The present article reports three cases of extrapulmonary TB which occurred in patients with RA undergoing treatment with biologics. The marked increase in the levels of neutrophil CD64 may provide important insight into the diagnosis of TB.
30262983 Identifying Reliable Diagnostic/Predictive Biomarkers for Rheumatoid Arthritis. 2018 INTRODUCTION AND OBJECTIVE: Elevated C-reactive protein is usually a good indicator of rheumatoid arthritis (RA); however, there are limitations that compromise its specificity and therefore there is an urgent need to identify more reliable diagnostic biomarkers to detect early stages of RA. In addition, identifying the correct therapeutic biomarker for the treatment of RA using methotrexate (MTX) would greatly increase the benefits experienced by the patients. MATERIALS AND METHODS: Primary normal synoviocytes human fibroblast-like synoviocytes (HFLS) and its phenotype rheumatic HFLS-RA cells were chosen for this study. The HFLS-RA-untreated and MTX-treated cells were subjected to microarray analysis. RESULTS: Microarray data identified 74 differentially expressed genes. These genes were mapped against an RA inflammatory pathway, shortlisting 10 candidate genes. Gene expression profiling of the 10 genes were studied. Fold change (FC) was calculated to determine the differential expression of the samples. DISCUSSION: The transcription profiles of the 10 candidate genes were highly induced in HFLS-RA cells compared with HFLS cells. However, on treating the HFLS-RA cells with MTX, the transcription profiles of these genes were highly downregulated. The most significant expression FC difference between HFLS and HFLS-RA (treated and untreated) was observed with HSPA6, MMP1, MMP13, and TNFSF10 genes. CONCLUSIONS: The data from this study suggest the use of HSPA6, MMP1, MMP13, and TNFSF10 gene expression profiles as potential diagnostic biomarkers. In addition, these gene profiles can help in predicting the therapeutic efficacy of MTX.
30723598 Survival Rate on a 10-Year Follow-Up of Total Wrist Replacement Implants: A 23-Patient Cas 2019 Feb Background  According to current literature, the estimated average survival rate for Remotion, the total wrist implants, is above 90% on an 8-year follow-up. We examined our series of Remotion to calculate its survival rate on a 10-year follow-up. Case Description  A total of 23 cases of total wrist implants were reviewed. The case series included 22 patients, 18 females and 4 males, of an average age of 55 years. The case series included 19 inflammatory rheumatic diseases, 3 Kienböck disease, and 1 posttraumatic arthrosis. Conclusion  The average survival rate of our case series was 95.7% on a 4-year follow-up, 91.3% on a 6-year follow-up, and 69% on a 10-year follow-up. On our review, the QuickDASH score, pain, wrist extension range of motion, and grip strength were improved postoperatively. No difference was shown between preoperative and postoperative values for wrist flexion, pronation, and supination. The case series included a septic case, treated by arthrodesis, and three total wrist implants displacements, two of which were treated by carpal implant, and the remaining one was treated by arthrodesis. Clinical Relevance  The survival rate of the total wrist replacement implant Remotion was estimated to be 69%.
30478988 Long noncoding RNAs in autoimmune diseases. 2019 Feb With the completion of the human genome project and further development of high-throughput genomic technologies, interest in long noncoding RNAs (lncRNAs), which are defined as non-protein-coding RNAs at least 200 nucleotides in length, has strongly increased, and lncRNAs have become a major research direction. Increasing evidence demonstrates that lncRNAs are closely related to human growth and development and to disease occurrence via various mechanisms. lncRNAs also play crucial roles in the differentiation and activation of immune cells, and their relationships with human autoimmune diseases have received increasing attention. The development of biotechnology has led to the gradual discovery of many potential lncRNA functions. In this review, we discuss various lncRNAs that have been implicated in different human autoimmune diseases, focusing on their clinical applications as potential biomarkers and therapeutic targets in the pathologies of diverse human autoimmune diseases. © 2018 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 107A: 468-475, 2019.
30369491 [A Case of Retro-Odontoid Pseudotumor in a Very Elderly Individual]. 2018 Oct Retro-odontoid pseudotumors are mainly caused by aging or rheumatoid arthritis. We treated a very elderly patient with retro-odontoid pseudotumor. A 92-year-old man was admitted with the chief complaints of difficulty walking and progressive numbness in the right upper and lower extremities. Neurological examination revealed muscle weakness and exaggerated tendon reflexes of the right upper and lower extremities, and disturbance in skilled motor activities of the fingers, bilaterally. He had no bladder or rectal disturbances. The Japanese Orthopaedic Association(JOA)score for cervical myelopathy was 10/17. Rheumatoid arthritis was interpreted as negative. Radiography of the neck showed no atlanto-axial instability. Cervical magnetic resonance(MR)imaging revealed a mass located posterior to the C2 odontoid process, severely compressing the cervical cord. The patient underwent a C1 laminectomy and C2 half laminectomy without fixation to achieve cord decompression. Postoperatively, muscle weakness in the right upper and lower extremities was remarkably improved, and gait disturbance was also improved. However, skilled motor activities of the fingers on the right hand during tasks such as writing letters, holding a cup, and using chopsticks, were not improved. JOA score was improved to 14/17. Postoperative radiography revealed no atlanto-axial instability and MR imaging revealed adequate decompression of the spinal canal. Laminectomy without fixation is recommended as an effective and less invasive treatment for retro-odontoid pseudotumor, especially in very elderly patients without atlanto-axial instability.
29605448 Neutrophils and redox stress in the pathogenesis of autoimmune disease. 2018 Sep Polymorphonuclear leukocytes, or neutrophils, are specialist phagocytic cells of the innate immune system. Their primary role is host defence against micro-organisms, which they kill via phagocytosis, followed by release of reactive oxygen species (ROS) and proteolytic enzymes within the phagosome. ROS are generated via the action of the NADPH oxidase (also known as NOX2), in a process termed the 'Respiratory Burst'. This process consumes large amounts of oxygen, which is converted into the highly-reactive superoxide radical O(2)(-) and H(2)O(2). Subsequent activation of myeloperoxidase (MPO) generates secondary oxidants and chloroamines that are highly microbiocidal in nature, which together with proteases such as elastase and gelatinase provide a toxic intra-phagosomal environment able to kill a broad range of micro-organisms. However, under certain circumstances such as during an auto-immune response, neutrophils can be triggered to release ROS and proteases extracellularly causing damage to host tissues, modification of host proteins, lipids and DNA and dysregulation of oxidative homeostasis. This review describes the range of ROS species produced by human neutrophils with a focus on the implications of neutrophil redox products in autoimmune inflammation.
30652043 Rheumatoid Meningoencephalitis: A Feared Condition in the Era of TNF Blockers. 2018 Central nervous system (CNS) involvement in rheumatoid arthritis (RA) is uncommon, and most of the times, it is secondary to vasculitic processes or extra-articular rheumatoid nodules. Meningeal involvement is extremely rare. In the literature, there are a few case reports, series, and retrospective studies which have demonstrated the association of rheumatoid (aseptic) meningoencephalitis after starting tumor necrosis factor (TNF) inhibitors. We present a case of rheumatoid meningoencephalitis (RME) in a 52-year-old male with a history of RA on adalimumab who presented with headaches associated with motor and sensory deficits, all of which resolved after this diagnosis was achieved and received appropriate therapy with high-dose glucocorticoids. We also present an update with high yield points summarizing clinical features, diagnostic workup, and management of RME. Finally, we post a literature review of relevant CNS rheumatoid disease in patients with and without exposure to TNF inhibitors.
29474901 Arachidonic acid metabonomics study for understanding therapeutic mechanism of Huo Luo Xia 2018 May 10 ETHNOPHARMACOLOGICAL RELEVANCE: Huo Luo Xiao Ling Dan (HLXLD), a traditional Chinese medicine (TCM), is commonly used for the treatment of rheumatoid arthritis (RA). AIM OF THE STUDY: To explore the potential therapeutic mechanism of HLXLD on anti-inflammatory activity. MATERIALS AND METHODS: A metabolomic approach based on UFLC-MS/MS to profile arachidonic acid (AA) metabolic changes was used. The cyclooxygenase (COX) and lipoxygenase (LOX) catalyzed metabolites in plasma were quantified on 7, 14, 21, and 28 days after the rats injected with Complete Freund's adjuvant and orally administrated with HLXLD, methotrexate and dexamethasone in parallel as the positive control drugs. RESULTS: Nineteen metabolites involved in COX and LOX pathways in RA model group were significant increased compared with normal group (P < 0.05), including 12-hydroxyeicosatetraenoic acid (12-HETE), 15-HETE, 8-HETE, leukotriene B(4)(LTB(4)), prostaglandin E(2) (PGE(2)), PGI(2), PGD(2), PGF(2α), thromboxane B(2) (TXB(2)), etc. From day 7 to day 28, the trajectory direction of HLXLD group and positive control groups gradually moved towards the initial space, and the concentrations of AA and its metabolites after HLXLD treatment were significantly reduced in dual pathways compared to control groups. CONCLUSION: HLXLD induced a substantial change in the AA metabolic profiles through refrain the expression of COX and LOX. The present investigation also highlights that distinct ingredients of this formula tend to inhibit different target to achieve a therapeutic effect.
30380700 Involvement of Aquaporins in the Pathogenesis, Diagnosis and Treatment of Sjögren's Syndr 2018 Oct 30 Sjögren's syndrome (SS) is a chronic autoimmune disease characterized by lymphocytic infiltration of salivary and lacrimal glands resulting in diminished production of saliva and tears. The pathophysiology of SS has not yet been fully deciphered. Classically it has been postulated that sicca symptoms in SS patients are a double step process whereby lymphocytic infiltration of lacrimal and salivary glands (SG) is followed by epithelial cell destruction resulting in keratoconjunctivitis sicca and xerostomia. Recent advances in the field of the pathophysiology of SS have brought in new players, such as aquaporins (AQPs) and anti AQPs autoantibodies that could explain underlying mechanistic processes and unveil new pathophysiological pathways offering a deeper understanding of the disease. In this review, we delineate the link between the AQP and SS, focusing on salivary glands, and discuss the role of AQPs in the treatment of SS-induced xerostomia.
29750331 Salivary-gland-protective regulatory T-cell dysfunction underlies female-specific sialaden 2018 Oct Immune cell-mediated destruction of salivary glands is a hallmark feature of Sjögren syndrome. Similar to the female predominance in humans, female non-obese diabetic (NOD) mice develop spontaneous salivary gland autoimmunity. However, in both humans and mice it is unclear what factors contribute to the initial immune infiltration of the salivary glands. Here, we used an adoptive transfer model of Sjögren syndrome to determine if female mice harbor a sex-specific defect in salivary-gland-protective regulatory T (Treg) cells. Transfer of cervical lymph node (LN) cells from female NOD mice into sex-matched NOD-severe combined immunodeficient (SCID) recipients resulted in sialadenitis, regardless of the presence or absence of Treg cells. In contrast, transfer of cervical LN cells from male NOD mice into sex-matched NOD-SCID recipients only resulted in sialadenitis when Treg cells were depleted before transfer, suggesting that male NOD mice have functional salivary-gland-protective Treg cells. Notably, the host environment affected the ability of Treg cells to prevent sialadenitis with testosterone promoting salivary gland protection. Treg cells from male mice did not protect against sialadenitis in female recipients. Testosterone treatment of female recipients of bulk cervical LN cells decreased sialadenitis, and Treg cells from female mice were capable of protecting against development of sialadenitis in male recipients. Hence, our data demonstrate that female NOD mice develop sialadenitis through a defect in salivary-gland-protective Treg cells that can be reversed in the presence of testosterone.
28437595 Natural History and Predictors of Progression to Sjögren's Syndrome Among Participants of 2018 Feb OBJECTIVE: To explore changes in the phenotypic features of Sjögren's syndrome (SS), and in SS status among participants in the Sjögren's International Collaborative Clinical Alliance (SICCA) registry over a 2-3-year interval. METHODS: All participants in the SICCA registry who were found to have any objective measures of salivary hypofunction, dry eye, focal lymphocytic sialadenitis in minor salivary gland biopsy, or anti-SSA/SSB antibodies were recalled over a window of 2 to 3 years after their baseline examinations to repeat all clinical examinations and specimen collections to determine whether there was any change in phenotypic features and in SS status. RESULTS: As of September 15, 2013, a total of 3,514 participants had enrolled in SICCA, and among 3,310 eligible, 771 presented for a followup visit. Among participants found to have SS using the 2012 American College of Rheumatology (ACR) classification criteria, 93% again met the criteria after 2 to 3 years, and this proportion was 89% when using the 2016 ACR/European League Against Rheumatism (EULAR) criteria. Among those who did not meet ACR or ACR/EULAR criteria at baseline, 9% and 8%, respectively, had progressed and met them at followup. Those with hypergammaglobulinemia and hypocomplementemia at study entry were, respectively, 4 and 6 times more likely to progress to SS by ACR criteria than those without these characteristics (95% confidence interval 1.5-10.1 and 1.8-20.4, respectively). CONCLUSION: While there was stability over a 2-3-year period of both individual phenotypic features of SS and of SS status, hypergammaglobulinemia and hypocomplementemia at study entry were predictive of progression to SS.
29879064 Primary Sjogren syndrome diagnosed simultaneously with localized amyloidosis of the lacrim 2018 Jun INTRODUCTION: Amyloidosis accompanied by Sjögren's syndrome (SS) has been reported to occur primarily in the skin, lungs, tongue, and mammary gland. However, SS in association with secondary amyloidosis is rarely reported, and knowledge of its relevance is inadequate. Here we report a case of primary SS diagnosed simultaneously with localized amyloidosis of the lacrimal gland. CASE PRESENTATION: A 45-year-old woman complaining of a left eyelid mass was referred to the hospital and was diagnosed with localized amyloidosis after excisional biopsy. She was then referred to the rheumatology department for additional evaluation for amyloidosis. Subsequently, her diagnosis was primary SS based on the presented symptoms and results of the Schirmer test, serologic testing, and minor salivary gland biopsy. Pilocarpine (10 mg/d) and hydroxychloroquine (200 mg/d) were initiated for the treatment of SS. Six months after the initial diagnosis, the dry eyes and mouth did not worsen and no masses suggestive of localized amyloidosis were reported. CONCLUSION: This is a rare case of amyloidosis, localized to the lacrimal gland, with SS. Therefore, despite its rarity, physicians should be aware of the potential coexistence of secondary amyloidosis, even in the localized form, in patients with SS.
29977932 MicroRNA in Sjögren's Syndrome: Their Potential Roles in Pathogenesis and Diagnosis. 2018 Sjögren's syndrome (SS) or sicca syndrome was described by Swedish ophthalmologist Sjögren in the year 1933 for the first time. The etiology of the SS is multifunctional and includes a combination of genetic predisposition and environmental as well as epigenetic factors. It is an autoimmune disease characterized by features of systemic autoimmunity, dysfunction, and inflammation in the exocrine glands (mainly salivary and lacrimal glands) and lymphocytic infiltration of exocrine glands. In fact, the involvement of lacrimal and salivary glands results in the typical features of dry eye and salivary dysfunction (xerostomia). Only in one-third of the patients also present systemic extraglandular manifestations. T cells were originally considered to play the initiating role in the autoimmune process, while B cells were restricted to autoantibody production. In recent years, it is understood that the roles of B cells are multiple. Moreover, autoantibodies and blood B cell analysis are major contributors to a clinical diagnosis of Sjögren's syndrome. Recently, there has been rising interest in microRNA implication in autoimmunity. Unfortunately, to date, there are only a few studies that have investigated their participation in SS etiopathogenesis. The purpose of this work is to gather the data present in the literature to clarify this complex topic.