ArticleProceedings of the National Academy of Sciences of the United States of America2026
Failure of early B cell tolerance and possible BCR signaling dysregulation underlie NF155-mediated autoimmune nodopathies.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Failure of early B cell tolerance and possible BCR signaling dysregulation underlie NF155-mediated autoimmune nodopathies.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Clinical utility of human leukocyte antigen genotyping and immunoglobulin G4 autoantibody testing in autoimmune neurological diseases: A focused minireview.World journal of biological chemistry · 2026Review
- The immune microenvironment and population heterogeneity in myasthenia gravis: implications for precision therapeutics.Frontiers in immunology · 2026Review
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16 authors.
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Abstract
Autoimmune nodopathies (AINs) are rare acquired autoimmune neuropathies with distinct clinical features and circulating autoantibodies, often of the immunoglobulin G4 (IgG4) subclass, targeting proteins at the node of Ranvier. Defects in B cell tolerance checkpoints have been implicated in several autoimmune diseases, including MuSK-positive myasthenia gravis, another IgG4 autoantibody-mediated disease. Here, we investigated whether tolerance defects exist in neurofascin-155-mediated AIN (NF155-AIN), using a well-established assay, by generating recombinant antibodies from new emigrant (NE) and mature naive (MN) B cells from three NF155-AIN patients, and tested them for polyreactivity and autoreactivity. Additionally, we analyzed the transcriptome of peripheral blood mononuclear cells, with a particular focus on naive B cells and CD4+ T cells at the single-cell level, and characterized cell-cell interactions. NF155-AIN patients have an elevated frequency of polyreactive B cells in the NE (37.4% compared to 9.7% in healthy controls (HCs),
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