ArticleJournal of translational autoimmunity2025
The antibody repertoire of autoimmune sensory neuronopathies targets pathways of the innate and adaptive immune system. An autoantigenomic approach.
Article in Journal of translational autoimmunity, 2025. 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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Who cites it
1 citing paper in PubMed.
- Mechanisms of autoimmune-mediated paraneoplastic syndromes: immune tolerance and disease pathogenesis.Frontiers in immunology · 2025Review
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8 authors.
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Abstract
Sensory neuronopathies (SNN) encompass diverse etiologies, with autoimmunity playing a major role through both cellular and humoral responses. To investigate the humoral autoantibody repertoire in autoimmune SNN, we conducted a retrospective cohort study using large Human Proteome-wide protein microarrays (HuProt 3.1, HuProt 4.0, ProtoArrays). We specifically analyzed immune system pathways targeted within the autoantigen repertoire (the autoantigenome). We included 131 participants: 44 patients with non-paraneoplastic autoimmune SNN (12 with anti-FGFR3 and/or anti-AGO antibodies), 8 with paraneoplastic SNN, and 79 controls. Findings were validated in an independent cohort of 16 SNN patients. Overrepresentation of immune-system-related proteins was assessed using the Reactome database, and serum levels of IFN-γ and IL-6 were measured with the Bio-Plex Pro™ Reagent Kit. Autoimmune SNN sera interact with significantly more immune system proteins than healthy controls (ProtoArrays: 271/863 vs. 14/863, HuProt: 112/1694 vs. 39/1694, both p < 0.0001). Overrepresentation was observed across all major immune sub-pathways, including innate and adaptive immune responses as well as cytokine signaling. Anti-FGFR3-positive SNN patients showed more frequent reactivity to immune system proteins than anti-FGFR3-negative ones. The independent SNN cohort validated the overrepresentation of targeted immune system pathways. Validation with dot blot and ELISA confirmed reactivity to TRIM21 and IL-6 and identified anti-IFN-γ-positive SNN patients. IFN-γ levels correlated weakly with levels of anti-IFN-γ antibodies (Pearson's
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