Systemic Lupus Erythematosus Research

This study analyzes the virome in SLE patients and controls, finding higher viral positivity in patients and suggesting viral infections may worsen disease severity.

This study uses engineered human cardiac tissues to show how SLE autoantibodies affect myocardial injury through distinct binding patterns and functional effects on cardiac cells.

The paper identifies functional regulatory SNPs in SLE risk loci by testing their impact on transcription factor binding and gene expression.

This study shows that CD11b activation reduces TLR7-driven inflammation and protects against lupus nephritis through mechanisms involving suPAR suppression and immune complex reduction.

This study identifies key regions and binding modes of beta-2-glycoprotein I domain V interacting with anionic membranes, important for antiphospholipid syndrome pathogenesis.

This study shows that LSP1 deficiency in B cells leads to myeloid-like traits and autoantibody production, accelerating lupus in mice and correlating with reduced LSP1 in lupus patients.

This study shows that MEK1/2-ERK1/2 inhibition prevents diffuse alveolar hemorrhage in lupus-prone mice by reducing endothelial injury and restoring hemostasis.

The paper uses immunophenotyping to identify patient subgroups in systemic autoimmune diseases, revealing shared immunophenotypes and cytokine signatures across different diagnoses.

This study identifies epigenetic and transcriptomic changes in SLE monocyte subsets, linking them to disease activity and function.

This paper presents a post-GWAS analysis pipeline to identify functional variants and target genes for SLE using integrative genomic and epigenomic data.

This study shows that Xist ribonucleoprotein complexes drive sex-biased autoimmunity in males, leading to autoimmune pathology and reprogramming of immune cells to resemble female patterns.

The paper shows that dietary tryptophan and genetic factors shape gut microbiota, which in turn influence autoimmune activation in lupus.

The paper identifies Fibronectin 1 as a biomarker for obstetric antiphospholipid syndrome through transcriptomic and protein expression analysis.

This study examines T cell exhaustion markers in SLE, finding that CXCR5+ CD8 T cells express high IFN-gamma and Tim3, suggesting a role in autoimmune progression and tolerance.

The paper identifies cell-specific transposable element (TE) gene expression associations with SLE phenotypes, finding 731 differentially expressed TEs linked to antiviral pathways and IFN signaling.

This paper applies a locus-based test called OASIS to GWAS datasets from European and Chinese populations to identify 35 common non-HLA SLE genes and their associated pathways.

This study identifies epigenetic differences in SLE linked to genetics, transcription, and serology, revealing novel drug targets and pathways.

The paper identifies disease genes and pathways in systemic lupus erythematosus by analyzing DNA methylation differences in blood cells, finding distinct patterns in T and B cells.

The paper identifies epigenetic differences in B cells from treatment-naive pediatric lupus patients compared to healthy children, showing distinct chromatin accessibility patterns and potential regulatory roles in disease.

The paper uses rule-based machine learning to identify gene expression subtypes in paediatric SLE, revealing gene networks associated with disease activity and immune pathways.

The paper identifies a novel risk variant rs1047643 and its association with B cell-specific super-enhancer activity in systemic lupus erythematosus through multi-omics analysis.

This study identifies cell-type-specific transcriptomic signatures associated with SLE disease establishment and exacerbation, highlighting their clinical relevance and potential limitations in capturing genetic risk factors.

The paper uses single-cell multi-omics to analyze T and NK cells in SLE patients, identifying IFN-driven changes and novel biomarkers.

This paper identifies IFN-driven cross-talk between immune cell types in SLE using gene expression analysis and a novel integrative method.

The paper identifies 482 SLE risk variants with enhancer activity and characterizes allelic regulatory mechanisms at 27 risk loci using MPRA.

This study identifies 38 novel SLE loci and shows genetic heterogeneity across ancestral groups, highlighting antibody production as a potential mechanism for disease disparities.

The paper identifies a non-coding genetic variant associated with SLE that regulates miR-146a expression through a cell-type specific enhancer.