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PubMedDate not supplied

Animal models of human systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a human autoimmune disease of unknown etiology. Clinical, serologic, immunologic, and pathologic findings are highly variable in different patients and at different times in the same patient. Murine and canine animal models of SLE have been found with clinicopathologic abnormalities resembling those observed in humans. Each animal model has unique characteristics; taken together they reflect the spectrum of disease in human SLE.Investigations in the animals have suggested that genetic, hormonal, immunologic, viral, and other environmental factors contribute to and modify the expression of disease. Where analogous studies are available for humans, the same factors have been found to modify disease expression in a similar fashion. Together, these studies have helped to clarify the multifactorial basis for SLE.The best characterized abnormalities are immunologic. These include excessive B cell function with the formation of large amounts of autoantibodies, and T cell abnormalities which include defects in T cell regulatory function as well as certain T cell effector functions.The animal models of SLE also serve as convenient test subjects for newer therapeutic modalities. It is hoped that further study of the animal models will provide a more rational approach to therapeutic modulation of disease in humans with SLE.

Animals↗
PubMed1975

Recent advances in the immunopathogenesis of systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a chronic multisystem inflammatory disease having definite etiologic associations with ethnic, genetic, viral and immunologic factors. Its pathologic hallmark, vasculitis, is currently felt to be the end result of an immune-complex mechanism. Several clinical and serologic variants of SLE are recognized including discoid lupus erythematosus (DLE), mixed connective tissue disease (MCTD) and drug-induced equivalents-such as procainamide-induced lupus (PIL). The distinguishing features of these variants as well as their prognosis and therapy are discussed in relation to recent developments in the immunopathogenesis of SLE.

Animals↗
PubMed1977

Hemolytic anemia and thrombocytopenic purpura: two related subsets of systemic lupus erythematosus.

Systemic lupus erythematosus patients who develop hemolytic anemia or thrombocytopenic purpura differ from other lupus patients and are similar enough to be considered two related subsets with a more benign course. Thirty-one lupus patients with either or both these hemocytopenias were found to be significantly younger, more often males, and had less frequent fever, polyarthritis, serositis, cutaneous vasculitis, nephropathy, neurologic manifestations, and persistent hypocomplementemia than 62 lupus patients without any of these hemocytopenias. They also had lower index scores of overall disease severity and required less treatment. It seems important to subdivide lupus patients in subsets for therapeutic and prognostic purposes.

Adolescent↗
PubMed1978

Diagnosis and management of systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is not a rare disease. There are several common clinical signs which should alert the physician to a possible diagnosis of SLE and which should condition him to look for specific clinical and laboratory findings. In addition to simple screening tests, useful procedures include a search for antinuclear antibodies, lupus erythematosus (LE) cells, anti-DNA antibodies and low serum complement. Management is determined by the type of course encountered but most patients will do well under the care of their family physician.

Adult↗
PubMed2026

Mapping the plasma proteomic architecture of systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a heterogeneous systemic autoimmune disease, yet the molecular basis underlying this variability remains incompletely understood. We profiled the plasma proteome in 260 SLE patients and 86 healthy volunteers (HVs) using the SomaScan v4.1 platform, quantifying 7,288 analytes corresponding to 6,595 unique proteins. We identified 215 proteins that were robustly differentially abundant between SLE patients and HVs in both discovery (n = 207 SLE, n = 45 HVs) and validation sets (n = 53 SLE, n = 41 HVs). Within-cases analyses identified 421 proteins associated with disease activity. Network-based clustering delineated correlated protein modules, including an interferon-associated (IFN-associated) module and a kidney-associated module. Autoantibody-stratified analyses further uncovered distinct proteomic endotypes; positivity for antibodies targeting RNA-binding proteins (anti-Sm, anti-Ro-60, anti-RNP68, anti-RNP-A) was associated with increased IFN-stimulated protein levels (e.g., MX1, ISG15, and CXCL10), independent of disease activity. Anti-Sm, anti-RNP-A, and anti-Ro52 antibodies were associated with reduced plasma levels of their respective autoantigens. Anti-dsDNA antibodies were associated with elevated levels of CD40 ligand (CD40LG) and the neutrophil protease, proteinase-3. Moreover, we identified an association between CD40LG and disease activity specific to the anti-dsDNA-positive subgroup. Together, these data define plasma protein signatures of SLE and disease activity, highlight autoantibody-specific molecular phenotypes, and provide a basis for precision medicine.

Humans↗
PubMed2026

The Multi-Omics Landscape of Enzymatic Alterations in Systemic Lupus Erythematosus.

OBJECTIVE: Systemic lupus erythematosus (SLE) is an autoimmune disease closely associated with enzyme dysfunction, yet its underlying molecular mechanisms remain incompletely understood. This study aims to characterize enzyme-network alterations associated with SLE status and disease activity and to identify candidate molecules with potential clinical relevance. METHODS: We integrated proteomic and phosphoproteomic data from peripheral blood mononuclear cells (PBMCs) of 130 SLE patients and 90 healthy controls (HC), along with transcriptomic data from 1461 SLE patients. Through systematic analysis of key enzyme phosphorylation sites, upstream transcription factors (TFs), and computationally prioritized candidate compounds, we sought to characterize enzyme-centered regulatory associations. RESULTS: Integrated proteomic and phosphoproteomic analyses revealed significant metabolic and signaling pathway disturbances, along with distinct phosphorylation patterns in SLE immune cells. Multiple SLE-associated and disease-activity-associated candidate molecules were identified. Regulatory network analysis uncovered an upstream transcription factor cluster centered around STAT1. Computational drug screening identified computationally prioritized candidate compounds with multi-gene DSigDB associations, which require further clinical safety evaluation and experimental validation. CONCLUSIONS: This study constructs a molecular map of SLE, highlighting associations between enzyme-network alterations, catalytic dysregulation, and SLE-related immune molecular signatures, and identifies candidate molecules for future clinical and functional evaluation.

Humans↗
PubMed2026

Integrated multi-omics profiling identifies aging-related molecular signatures and convergent interferon signaling in systemic lupus erythematosus.

BACKGROUND: Systemic lupus erythematosus (SLE) is characterized by chronic immune activation and molecular alterations that overlap with aging-related biological processes. However, how these alterations are organized across molecular layers and whether they converge on shared regulatory networks remain incompletely understood. METHODS: We performed an integrative multi-omics analysis combining in-house proteomic and phosphoproteomic data from 130 patients with SLE and 90 healthy controls (HCs) and publicly available transcriptomic datasets comprising 1,461 SLE patients. Proteins and phosphorylation sites were annotated using established aging-related gene resources. Differential protein abundance and phosphorylation changes were analyzed across disease-status and disease-activity comparisons. Nominal P-value thresholds were used for exploratory feature selection, whereas FDR-adjusted P values were used to assess robustness after multiple-testing correction. Kinase-substrate enrichment, transcription factor annotation, and cell-type-resolved transcriptomic comparison were used to explore potential regulatory programs. RESULTS: We identified 128 nominally altered proteins annotated to aging-related biological processes, including genomic instability, mitochondrial dysfunction, and epigenetic alterations. Phosphoproteomic analysis revealed 36 nominally altered phosphorylation sites, including previously unreported sites in IFI16 (S153, S780) and PKCδ (S507, S664). Clustering analysis demonstrated heterogeneous protein co-regulation patterns across disease states. Kinase activity inference suggested altered activity of TBK1 and IKKβ. TF analysis further highlighted STAT1, RELA, and PML as potential central nodes within the inferred regulatory network. Notably, these multi-omic alterations were not randomly distributed but showed convergence toward shared signaling pathways, particularly those related to interferon responses. CONCLUSIONS: This integrative multi-omics study identifies inflammatory and interferon-dominated molecular alterations in SLE PBMCs that overlap with aging-related biological processes and converge on shared regulatory networks. These findings provide a hypothesis-generating framework for investigating the intersection between chronic immune activation and aging-related molecular remodeling in SLE.

Humans↗
PubMed1977

Immunoglobulin classes of DNA binding activity in serum and skin in systemic lupus erythematosus.

36 systemic lupus erythematosus patients with native DNA binding activity (nDNA-BA) in the serum and subepidermal immunoglobulin deposits were studied to determine the relationship of the immunoglobulin (Ig) class distribution of serum nDNA-BA to the clinical characteristics of their disease and to the Ig class present at the dermal-epidermal junction (DEJ). The patients with predominantly (86-98%) IgM nDNA-BA in the serum had less active disease, mild or no renal involvement, and longer survival than those with predominantly (51-95%) IgG nDNA-BA in the serum. Renal biopsies in eight patients with predominantly IgM nDNA-BA in the serum showed relatively benign histologic changes in the kidney. In contrast, renal tissue from 23 patients with predominantly IgG nDNA-BA showed more severe histologic changes. All patients had multiple skin biopsies. Patients with predominantly IgM nDNA-BA consistently had only IgM at the DEJ. Patients with predominantly IgG nDNA-BA had IgG, usually in association with IgM, at the DEJ. The findings demonstrate that a minority of systemic lupus erythematosus patients may exhibit a limited anti-nDNA response characterized by the presence of chiefly IgM nDNA-BA in the serum and that this is reflected by the presence of mild disease and IgM alone at the DEJ. The development of IgG nDNA-BA is associated with more severe and active disease.

Centrifugation, Density Gradient↗
PubMed2026

Integrative post-GWAS analysis prioritizes immune regulatory pathways and candidate effector signals in systemic lupus erythematosus.

BACKGROUND: Systemic lupus erythematosus (SLE) has a complex polygenic architecture, but translating genome-wide association signals into biologically interpretable candidates remains challenging. We applied an integrative post-GWAS framework to refine SLE-associated loci and prioritize candidate regulatory mechanisms. METHODS: European-ancestry SLE GWAS summary statistics from FinnGen and Bentham et al. were meta-analysed, comprising 8417 cases and 354,277 controls. After quality filtering, 6,782,131 SNPs were retained. Downstream analyses included LAVA regional prioritization, Bayesian colocalization with GTEx v8 whole-blood and spleen eQTLs, independent replication in the Julià et al. Spanish cohort, pathway enrichment, bivariate LAVA cross-trait local genetic correlation, and therapeutic annotation. RESULTS: The discovery meta-analysis identified 46 genome-wide significant SLE-associated loci, including putative novel signals requiring database/literature qualification. LAVA identified 14 candidate index variants across 12 high-confidence regions, of which nine index variants were retained as the primary prioritized set based on LAVA support and/or convergent regulatory evidence. The strongest association mapped to the chr6p21.3/MHC region (rs389884), where four genes showed colocalization support, including CLIC1 in whole blood and C4A in spleen. Because the chr6p21.3/MHC rs389884 region lead variant was unavailable for replication and no suitable proxy was identified, this signal was interpreted as an emerging candidate for functional validation rather than a replicated causal signal. Seven available variants replicated with concordant effects. An exploratory Roadmap immune chromatin-state overlap analysis placed 15 of 45 non-MHC lead variants (33.3%) directly, and 34 of 45 (75.6%) within ±10 kb, in active immune enhancer/promoter states. Pathway analyses highlighted type I interferon, JAK-STAT signaling, cytokine regulation, and antigen presentation, while bivariate LAVA analyses supported shared local genetic architecture with rheumatoid arthritis, systemic sclerosis, and Sjögren syndrome. CONCLUSIONS: This integrative post-GWAS analysis refines SLE association signals into biologically interpretable candidate regions and supports interferon and JAK-STAT signaling as central genetically supported pathways in SLE.

CLIC1↗
PubMed1975

[Morphologic changes in the chorio-allantoic membrane and organs of chick embryos inoculated with blood of patients with systemic lupus erythematosus (concerning the viral etiology of systemic lupus erythematosus)].

Morphological studies of 14 chorionallantoic membranes and organs of chick embryos which had been infected on the 7--8th day of incubation with leucocytic mass from patients with systemic lupus erythematosus were carried out. Corresponding virological and morphological control studies were performed. The changes observed were repeatedly reproduced in multiple inoculations (from the 2nd to the 16th passage). Apart from morphological changes, which may be listed among general pathological processes (impairment of the circulation, dystrophy, proliferation), changes testifying to a possible cytopathic effect disintegration of nuclei, formation of gigantic cells and multinuclear symplasts were also noted. The most pronounced changes, both in the chorionallantoic membrane and in internal organs, were observed on the 3rd--5th passage and on the 3rd--5th day of incubation following inoculation. They correlated with the clinical activity of the process in patients from whom the blood for inoculation had been taken. The data obtained justify the assumption concerning the existence in the blood of the patients with systemic lupus erythematosus a transplantable agent producing a cytopathic action, and may be considered as a new indirect corroborative evidence in favour of the concept of the viral nature of systemic lupus erythematosus.

Animals↗
PubMedDate not supplied

Myocardial involvement in systemic lupus erythematosus and systemic sclerosis--pulsed Doppler echocardiographic evaluation of left ventricular diastolic function.

Myocardial involvement (MI) in connective tissue diseases is commonly found at autopsy but seldom recognized clinically. To assess the subclinical MI, the left ventricular (LV) diastolic function was studied in 16 patients with systemic lupus erythematosus (SLE) and 15 patients with systemic sclerosis (SSc) by means of pulsed Doppler echocardiography. Patients with abnormal LV systolic function were not included. A control group (C) included 16 sex and age-matched healthy subjects. The parameters analyzed were: peak early diastolic flow velocity (E), peak late diastolic flow velocity (A), E/A ratio, isovolumic relaxation time (IRT). LV diastolic function was found impaired in SLE and SSc patients even when systolic function was normal as could be demonstrated by pulsed Doppler echocardiography.

Cardiomyopathies↗
PubMed1979

Antibodies to small nuclear RNAs complexed with proteins are produced by patients with systemic lupus erythematosus.

Patients with systemic lupus erythematosus often possess antibodies against two nuclear antigens called Sm and RNP (ribonucleoprotein). We have established the molecular identity of these antigens by analyzing immune precipitates of nuclear extracts from mouse Ehrlich ascites cells labeled with (32)P and (35)S. Anti-Sm serum selectively precipitates six small nuclear RNA molecules (snRNAs); anti-RNP serum reacts with only two of these; and a third serum, characterized as mostly anti-RNP, precipitates a subset of three snRNA bands. Three of the six RNAs are identified by fingerprint analysis as the previously characterized and highly abundant nucleoplasmic snRNA species U1a (171 nucleotides), U1b, and U2 (196 nucleotides). The other three RNAs (U4, U5, and U6) likewise are uridine rich and contain modified nucleotides, but they are smaller, with lengths of about 145, 120, and 95 residues, respectively. Each of the six snRNAs is complexed with and apparently antigenic by virtue of association with specific proteins. All three sera precipitate an identical complement of seven different polypeptides ranging in molecular weight from 12,000 to 35,000; these proteins are abundant in nuclear extracts, but are neither histones nor the major polypeptides comprising the 30S heterogeneous nuclear RNP particles of mammalian nuclei. Our data argue that each of the six snRNAs exists in a separate small nuclear ribonucleoprotein (snRNP) complex with a total molecular weight of about 175,000. We find that human antisera also precipitate snRNAs from a wide range of vertebrate species and from arthropods. We discuss the antigenic snRNPs in relation to the published literature on snRNAs and nuclear RNPs and consider possible functions of snRNPs in nuclear processes.

Antibodies, Antinuclear↗