ArticleFrontiers in immunology2026
Comorbidity risk characteristics of rheumatoid arthritis in the context of depression-associated lipid metabolism.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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6 authors.
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Abstract
Background: Rheumatoid arthritis (RA) and major depressive disorder (MDD) exhibit significant comorbidity, with shared pathological mechanisms such as inflammation and abnormal lipid metabolism. However, the specific molecular features and functional pathways linking the two diseases remain unclear. Methods: This study integrated public transcriptomic data from five MDD and five RA cohorts. Lipid metabolism-related module genes were screened in MDD cohorts and intersected with RA-upregulated differentially expressed genes to construct a candidate set. LASSO regression and machine learning (XGBoost, Random Forest) were used for feature selection and model construction. Functional exploration included protein-protein interaction network analysis, immune infiltration analysis, and multi-cohort validation. To experimentally test the proposed lipid-immune link and a potential neuron-to-synovium axis, we established an Results: A nine-gene lipid-immune signature (ANXA3, IL18, CD59, TNFSF13B, BMX, WASF1, SLC8A1, COMMD8, NXT2) was identified. It showed excellent discriminative performance in independent RA cohorts (AUC 0.86-1.00) but weaker performance in MDD cohorts (AUC 0.55-0.65). TNFSF13B, IL18, and CD59 were consistently identified as core hubs. The signature's expression correlated significantly with immune cell infiltration in RA. Critically, our Conclusion: This study identifies a conserved lipid-immune gene signature associated with the risk of MDD-RA comorbidity and provides multi-level validation encompassing bioinformatic prediction, clinical cohort correlation, and direct experimental evidence (qPCR, ELISA, WB). The signature may represent an immune-inflammatory state activated in a subset of MDD individuals that overlaps with RA pathology. Based on the hub genes, a "Lipid Metabolism - Membrane Microenvironment - Immune Inflammation" axis hypothesis is proposed. The experimentally demonstrated neuron-synovium paracrine axis, characterized by specific molecular changes (CD59, IL-6, MMP3), offers a novel and testable mechanistic conduit for cross-disease pathology, providing new molecular insights and directions for understanding psychiatric-immune comorbidity.
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