ArticleKidney diseases (Basel, Switzerland)
Immunoprofiling by CyTOF Uncovers Disease-Defining Peripheral Immune Signatures and Mechanistic Links to Renal Injury in IgA Nephropathy.
Article in Kidney diseases (Basel, Switzerland). 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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1 citing paper in PubMed.
- Inhibition of p65 NF-κB enhances production of galactose-deficient IgA1 through suppression ofbioRxiv : the preprint server for biology · 2026Article
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9 authors.
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Abstract
Introduction: The immunopathogenesis of IgA nephropathy (IgAN) involves mechanisms beyond B-cell dysregulation, yet the full spectrum and clinical relevance of peripheral immune alterations remain insufficiently defined. Methods: Peripheral blood from 7 IgAN patients and 3 healthy controls was analyzed by 30-marker mass cytometry (CyTOF), revealing 22 immune clusters across lymphoid and myeloid lineages. Independent flow cytometry validated CyTOF findings in 50 IgAN patients and 10 controls. Group differences were assessed by Mann-Whitney U test and associations with clinical measures via Spearman correlation. Results: CyTOF mapping revealed 22 immune clusters spanning lymphoid and myeloid lineages. Among these, two subsets showed a significant increase in IgAN: switched memory B cells (CD19 Conclusions: Our study delineates a peripheral immune signature of IgAN characterized by enhanced B-cell activation and cytotoxic T-cell responses, reflecting a dual-axis immune imbalance that may shape disease progression. These findings refine current immunopathogenic models and may guide future therapeutic research.
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