Systemic Lupus Erythematosus Research Research Articles

Analyzing systemic lupus erythematosus publications using neural network-based multi-label classification algorithms.

The heterogeneity in systemic lupus erythematosus research topics poses a challenge for the entire lupus community, from basic geneticists to clinical investigators. As such, it is critical for medical professionals to remain up to date on directions in lupus research and the main fields in which this research is being conducted (e.g., etiology, diagnosis, treatment, and outcomes). This article develops two multi-label text-classification models using Deep Neural Networks and Convolutional Neural Networks to classify the human-based adult-onset lupus–related articles in the PubMed database based on their abstract, keywords, and MeSH terms. During training evaluation, our models correctly indicated all relevant labels for 70% of the articles. The applied machine learning models (Deep Neural Network and Convolutional Neural Network) yielded a Micro-F1 score of 0.89, meaning that it successfully labeled the most relevant medical domains and types. In addition, these types of studies help the researchers be aware of the essential topics in this field, but due to difficulties in designing, the related studies are ignored or fade.

TRPC6 gene variants and neuropsychiatric lupus

Neuropsychiatric manifestations of systemic lupus erythematosus (NPSLE) influence patients' quality of life and their survival. Little is known about the pathophysiological bases of NPSLE and accordingly there are no specific therapeutic agents to be employed in this setting. Genetic research in systemic lupus erythematosus (SLE) is rapidly evolving as a tool to find clues about the pathogenic determinants of the disease and of its manifestations. Here, we describe the association of a single nucleotide polymorphic variant of the transient receptor potential cation channel, subfamily C, member 6 (TRPC6) gene with protection from the development of NPSLE in a cohort of 106 patients with SLE. TRPC6 is involved in the regulation of N-methyl-d-aspartate (NMDA) receptor signalling, a major player in post-ischemic neuronal injury and in the pathogenesis of NPSLE. TRPC6 genetic variants are promising candidate predictors of nervous system involvement in SLE, whereas the TRPC6 pathway might constitute a potential novel therapeutic target.

Beta-adducin and sodium-calcium exchanger 1 gene variants are associated with systemic lupus erythematosus and lupus nephritis.

Genetic research in systemic lupus erythematosus (SLE) is rapidly developing, and numerous sets of genes are being associated with specific clinical subphenotypes in the setting of SLE. On the other hand, basic science studies are revealing strong connections between salt-water balance and inflammation. The aim of this study was to evaluate whether variants of genes known to influence the individual susceptibility to hypertension also influence the renal function in a cohort of SLE patients with and without lupus nephritis (LN). This study is a case-control study with candidate gene approach. A total of 111 patients with SLE (50 with SLE without nephritis, 55 with LN and 6 with simple urinary sediment abnormalities) and 62 healthy controls (HC) were genotyped for NCX1 rs11893826 (NCX1a) and rs434082 (NCX1b) and ADD2 rs4984 SNPs. Patients with ADD2 CT genotype were protected from LN and skin involvement; ADD2 CC | NCX1a AA/AG genotypes were associated with the presence of anti-cardiolipin antibodies; NCX1a AA genotype was slightly more frequent in lupus patients than in HC and associated with relapse risk and higher creatinine in patients with LN. NCX1b GG patients with LN had increased chances to reach complete remission. NCX1b GG | NCX1a GG genotype is associated with joint involvement. ADD2 and NCX1 variants influence the risk and the clinical features of SLE and LN, highlighting their potential role in regulating systemic inflammation and/or the local response to immune-mediated injury.

Taking a closer look at biologic therapy for SLE

Clinical, basic and translational research in systemic lupus erythematosus are fast-moving fields. 2013 has seen the publication of some potentially landmark papers, which not only explore the potential of novel agents but also glean new insights from past trials.

Clinical research in systemic lupus erythematosus: immediate relevance to clinical practice

Systemic lupus erythematosus remains a challenge because of its diverse presentations, variable natural history, and lack of uniform response to treatment. True remission is very rare. Reliance on corticosteroid treatment leads to unwanted long-term toxicity. Great advances have been made in the early detection of lupus nephritis and in treatment. Greater appreciation of cognitive impairment and of lupus myelitis is now possible. Pregnancy risks are better characterized. However, the greatest unmet challenge remains atherosclerosis.

Genetics research in systemic lupus erythematosus for clinicians: methodology, progress, and controversies

Clinical journals are reporting genetic associations with systemic lupus erythematosus (SLE) with increasing frequency. Interpreting these studies is difficult for clinicians without rigorous training in epidemiology, statistics, and genetics. In this review, we discuss basic issues important to understanding and contextualizing new genetic association studies. We, therefore, highlight literature related to methodology as well as recent genetic discoveries in SLE. Functional single nucleotide polymorphisms (SNPs) and/or haplotypes have now been identified for ITGAM, PTPN22, and IRF5, and several additional loci have been highlighted in recent genome-wide association studies in SLE. Recent work also indicates that several regions within the extended major histocompatibility complex contribute independently to SLE risk. Evidence of additive statistical interaction has been found between IRF5 and TYK2, IRF5, and STAT4, and between NAT2 and exposure to tobacco smoke. Many new genes have been associated with SLE susceptibility, revealing insight into SLE pathophysiology. Current research is focusing on further refining the initial genetic association results and extending this work to non-European populations. Research is also expanding beyond SNP associations to investigate the contribution of copy number variants (CNVs) and DNA methylation to SLE risk.

Induction of immune tolerance by activation of CD8 + T suppressor/regulatory cells in lupus-prone mice

Multiple CD8 + suppressive T cell (Ts) subtypes are now recognized as essential regulators of the immune system that prevent autoimmunity through secretion of multiple cytokines and the subsequent inhibition of effector lymphocyte function. CD8 + Ts are an exciting area of study because of the possible therapeutic implications of inducing suppressive cells that are able to subdue or anergize autoimmune manifestations. Current research in systemic lupus erythematosus (SLE), a disease in which most effective therapies are widely immunosuppressive, is often focused on novel and highly targeted ways in which to treat this multiorgan disease. CD8 + Ts have been impaired in human and murine SLE. Our group and others have utilized tolerogenic peptides to induce and study CD8 + Ts to understand their function, as well as investigate a possible new SLE therapy. This review will discuss the similarities and differences in CD8 + Ts subsets, the concept of tolerance as a therapy, and the current understanding of CD8 + Ts in mouse SLE models.

Frontiers of SLE: Review of the 5th InternationalCongress of systemic lupus erythematosus, Cancun, Mexico, April 20–25, 1998

Objective: To review the recent advances in clinical and experimental research in systemic lupus erythematosus (SLE). Methods: Review of the 5th International Congress of SLE that took place inCancun, Mexico, on April 20–25, 1998. Results: The main topics presented at the conference are summarized. These include new findings about the genetics of SLE due to fine mapping of the patients' genes and lupus mouse models, the nucleosome as a major autoantigen in SLE, serving as an immunogen for pathogenic T helper and B cells and contributing to the development of lupus nephritis, abnormalities of apoptosis as a cause of SLE, and apoptotic mechanisms as a cause of autoimmunization. Other topics included the pathophysiologic role of anti-endothelial cell antibodies in lupus with central nervous system involvement, vasculitis, the thrombotic diathesis associated with the antiphospholipid syndrome, induction of endothelial cell apoptosis and its regulation by the idiotypic network, the penetration of antinuclear antibodies to the cytoplasm and nucleus and the subsequent interaction with cellular organelles, and new aspects in the antiphospholipid syndrome, including animal models of the disease and the importance of antibodies to beta-2-glycoprotein-I and prothrombin. Advances in the clinical aspects of SLE included clinical manifestations, diagnosis, pregnancy and neonatal SLE, infections, hormones, and treatment. Additionally, four “Lectures of A Lifetime,” entitled (1) What causes lupus? (2) From natural autoimmunity to autoimmune disease; (3) The idiotypic network and SLE; and (4) Late-stage morbidity and mortality in SLE-the role of accelerated atherosclerosis were presented. Conclusions: Recent advances provide new insights into the pathogenesis of SLE, as well as hope for novel therapeutic modalities and diagnostic measures. These offer the possibility of improving life quality and decreasing mortality from the disease and its complications.

Genetic and immunological mechanisms in the pathogenesis of systemic lupus erythematosus

Recent research in systemic lupus erythematosus and animal models of lupus has provided new insight into the pathogenesis of this complex autoimmune disease. Progress has been made towards understanding the genetic contributions to disease susceptibility and induction, as well as towards elucidation of the lymphocyte abnormalities involved in pathogenic autoantibody production.

New Directions for Research in Systemic Lupus Erythematosus

New Directions for Research in Systemic Lupus Erythematosus