ArticleFrontiers in immunology2025
Body weight in systemic lupus erythematosus is associated with disease activity and the adaptive immune system, independent of type I IFN.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed.
- Association of the FTO gene polymorphism with the features of the clinical course of tuberculosis infection.BMC infectious diseases · 2026Article
- Article
- The relationship between obesity and disease relapse in systemic lupus erythematosus: a retrospective cohort study using the LUNA registry.Frontiers in immunology · 2026Article
- Transcriptomic Analysis Reveals C-C Motif Chemokine Receptor 1 as a Critical Pathogenic Hub Linking Sjögren's Syndrome and Periodontitis.Current issues in molecular biology · 2025Article
- Body mass index distinctly modulates the associations between Alistipes and CRP/IL-6 in metabolic and lupus inflammatory features.PloS one · 2025Article
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6 authors.
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Abstract
Objective: To explore the relationship between physique and immunological disturbances in systemic lupus erythematosus (SLE), we analyzed the clinical, immunological and transcriptomic characteristics of patients with SLE in relation to body mass index (BMI). Methods: Clinical characteristics were obtained from patient charts, and serum cytokine levels were measured. Phenotypes and transcriptomes of peripheral immune cells from patients with SLE in the ImmuNexUT database were analyzed in relation to BMI. Results: Thirty-four SLE patients were included in the analysis. Fever and mucocutaneous symptoms were commonly observed in SLE patients with a low BMI. BMI was negatively correlated with the SLE disease activity (SLEDAI)-2K scores. Multiple regression analysis revealed that BMI was an independent explanatory variable for SLEDAI-2K scores, irrespective of anti-dsDNA antibody or complement levels. Although serum interferon (IFN)-alpha and IFN-gamma levels were negatively associated with BMI, causal mediation analysis showed that BMI had a direct effect on SLEDAI-2K scores, independent of IFN-alpha levels. Immunophenotyping indicated that BMI was primarily correlated with T cell subsets. BMI-related gene expression was mainly enriched in the regulatory T cells and B cell subsets. BMI was negatively correlated with several cellular metabolic pathways, including glucose metabolism-related pathways in Th1 and effector memory CD8 Conclusion: We characterized the clinical, immunological and transcriptomic profiles of SLE patients with varying BMI. As low BMI was identified as an independent parameter for explaining disease activity, cachexia is considered one of the systemic symptoms of active SLE. Additionally, BMI influenced the phenotypic and transcriptomic alterations of acquired immune cells, independent of IFN signaling. These findings provide insights into the pathogenesis of SLE.
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