Systemic Lupus Erythematosus Research

Autoantigen TRIM21 (Ro52) assembles pro-inflammatory immune complexes following lytic cell death

The paper shows TRIM21 becomes an autoantigen by forming pro-inflammatory immune complexes after lytic cell death, which are taken up by macrophages and drive inflammation.

Application of Engineered NK-92 Cell Extracellular Vesicles in the Treatment of Systemic Lupus Erythematosus

This study develops engineered NK-92 cell-derived extracellular vesicles targeting CD19 to treat SLE in mice, showing reduced B cells, improved renal function, and increased survival.

CNS diseases cerebrospinal fluid single-cell atlas reveals immune characteristics of neuropsychiatric systemic lupus erythematosus

The paper constructs a single-cell atlas of cerebrospinal fluid and blood from CNS diseases, revealing immune features of NPSLE and providing a public resource for future research.

Knockdown of the long isoform of the prolactin receptor selectively targets pathogenic immune cells and averts lupus nephritis

This study shows that knocking down the long isoform of the prolactin receptor reduces pathogenic immune cells and prevents lupus nephritis in SLE-prone mice.

Damaged glomeruli in proliferative pediatric lupus nephritis exhibit a C5a-C5aR1 induced fibrotic transcriptional program

The paper identifies a C5a-C5aR1 signaling pathway driving fibrosis in damaged glomeruli of pediatric lupus nephritis using spatial transcriptomics and bulk RNA-seq.

Deep immune profiling pinpoints cellular and molecular drivers of lupus immunopathology

The paper identifies novel cell states and molecular profiles in lupus patients using single-cell data, linking them to disease severity and treatment outcomes.

Single-cell level characterization of B cell depletion and repopulation following rituximab in systemic lupus erythematosus

This study uses single-cell profiling to track B cell depletion and repopulation in SLE patients after rituximab treatment, revealing changes in B cell subsets and immune cell dynamics.

Mechanistic insights into B-cell activation and autoreactivity regulation in active SLE and remission.

This study compares B-cell subsets in active SLE, remission, and healthy controls to identify immunological differences and potential therapeutic targets.

Elevated ferritin as a companion biomarker of myeloid-driven inflammation in RNP/Sm co-positive, treatment-resistant SLE endotype

This paper identifies an RNP/Sm co-positive SLE endotype with myeloid-driven inflammation, hyperferritinaemia, and treatment resistance, suggesting targeted therapies are needed.

Reduced late endosome/lysosome function promotes SLE through chronic PI3k activity and SHP-1/SHIP-1 defects

This study identifies reduced late endosome/lysosome function in SLE patients, linked to chronic PI3k activity and SHP-1/SHIP-1 defects, and suggests it as a potential biomarker.

IFN gamma-induced IRF1 synergizes with TLR7 signals to tune the IRF4-IRF8 axis and drive pathogenic effector B cell fate

The paper shows IRF1 regulates B cell fate by modulating the IRF4-IRF8 axis, promoting pathogenic effector B cells in SLE.

Early developmental placental defects and pregnancy loss in lupus mice expressing human TLR8

This study identifies huTLR8's role in placental defects and pregnancy loss in lupus mice, showing its involvement in immune dysregulation and inflammation.

Neutrophils impair B cell differentiation via mitochondrial and lipid metabolism in lupus.

This study shows neutrophil-derived mitochondrial DNA impairs B cell differentiation in lupus nephritis through oxidative stress and lipid metabolism disruption.

Ultraviolet B Induces Cutaneous Lupus Erythematosus by Triggering a Ribotoxic-Stress-Response-Dependent MIF-p38 Feedback Loop in Keratinocytes

This study identifies a UVB-induced MIF-p38 feedback loop in lupus keratinocytes that drives cutaneous lupus erythematosus and shows a microneedle patch targeting MIF can alleviate skin lesions.

An Advanced Humanized Systemic Lupus Erythematosus Model Enables Parallel Profiling of B Cell-Targeted Therapies

This study develops a humanized SLE model to compare B cell-targeted therapies, finding UCAR-T provides better renal and autoantibody reduction than TCEs despite higher toxicity.

Interleukin-36 upregulates type-I interferon responses in systemic lupus erythematosus by promoting the accumulation of self-nucleic acids

This study shows IL-36 promotes monocyte apoptosis and downregulates nucleic acid clearance, leading to self-nucleic acid accumulation and enhanced type-I IFN responses in SLE.

Dysregulation of U12-Type Splicing in Lupus Neutrophils

This study identifies dysregulated U12-type splicing in lupus neutrophils, linking it to impaired Nox activity and immune dysfunction.

Glycolysis inhibition functionally reprograms T follicular helper cells and reverses lupus

This study shows that inhibiting glycolysis with 2DG reduces TFH cell expansion and autoantibody production in lupus-prone mice, with potential therapeutic implications for SLE.

Antiphospholipid syndrome (APS) is a platelet factor 4 (PF4)-centric immunothrombotic disorder

This study identifies PF4 as a central factor in APS by showing it bridges {beta}2GPI to NETs, forming prothrombotic complexes that are targeted by APS antibodies.

Neutrophil Transcriptomics in SLE: Exploring Intrinsic, Ex Vivo Adaptation, and CAR T-Cell Therapy-Induced Changes

This study identifies transcriptomic differences in SLE neutrophils, shows shared ex vivo adaptation with healthy cells, and demonstrates CAR T-cell therapy can reset neutrophil gene expression toward healthy patterns.

CD8 T lymphocytes infiltrate the kidneys and correlate with disease progression in B6.NZMSle1/Sle2/Sle3 lupus mice

This study shows that CD8 T cells infiltrate kidneys in lupus mice and correlate with disease progression, but do not dominate over CD4 T cells.

Autoantibody origins in lupus and in relapse post CAR-T therapy

The paper shows that autoantibody production in lupus is sustained by continuous B cell differentiation, not long-lived plasma cells, and relapse after CAR-T therapy occurs via new B cells.

Hippocampal multi-layered RNAseq prioritizes oligodendrocyte dysfunction over immune-driven neuroinflammation in neurolupus pathogenesis

The paper identifies oligodendrocyte dysfunction as a key driver of NPSLE pathogenesis, contrasting with immune-driven inflammation in the hippocampus of MRL/Lpr mice.

Molecular signature of neutrophils in antiphospholipid syndrome based on epigenomic and transcriptome analysis

This study identifies CCL5 and ITK as key genes in neutrophils associated with antiphospholipid syndrome through epigenomic and transcriptome analysis, linking them to multiple signaling pathways and potential drug targets.

Mitochondrial instability contributes to IFN-driven heart disease.

This study shows chronic IFN exposure impairs heart function by causing mitochondrial stress, mtDNA release, and a self-sustaining inflammatory loop in cardiomyocytes.

A Computational Pipeline for Stratifying Autoimmune Patients Using Binary Antibody Data

This paper introduces a computational pipeline that stratifies autoimmune patients using binary antibody data, demonstrating its utility in two autoimmune disorders.

Establishment of a Systemic Lupus Erythematosus Mouse Model in Humanized CD3/CD19 Mice and Evaluation of the Efficacy of a Human Bispecific Antibody

This paper establishes a humanized CD3/CD19 mouse model of SLE and evaluates the efficacy of a human bispecific antibody in treating the disease.

A population-scale atlas of blood and tissue in lupus nephritis

A single-cell atlas of blood and tissue samples from lupus nephritis patients and healthy controls identifies stromal and immune populations, including scar-associated macrophages, which correlate with disease activity.

TASL is required for age-related B cell formation and autoimmunity

This study shows TASL is essential for age-related B cell formation and autoimmunity in a lupus mouse model, but not for B cell development.

Mitochondrial Bioenergetic Failure in SLE Immunocytes: Targeting Fitness for Therapy

This study identifies mitochondrial bioenergetic failure in SLE immunocytes, showing reduced OXPHOS across multiple immune subsets and proposes targeting mitochondrial fitness for therapy.