ArticleBrain and behavior2023
S100A6 participates in initiation of autoimmune encephalitis and is under epigenetic control.
Article in Brain and behavior, 2023. 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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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- Multifaceted roles of S100A6 in neurological disorders: expression, interaction networks, and clinical implications.Frontiers in pharmacology · 2026Review
- Scar-associated macrophages and biliary epithelial cells interaction exacerbates hepatic fibrosis in biliary atresia.Pediatric research · 2026Article
- Rare Variants of Immune-Related Genes Increase Susceptibility to Autoimmune Encephalitis: An Association Study.Neurology international · 2025Article
- Dissection of the trans-endocytosis and signal inhibition functions of CTLA-4 through the study of a disease-associated Y139C mutation.Cellular & molecular immunology · 2025Article
- S100A6 participates in initiation of autoimmune encephalitis and is under epigenetic control.Brain and behavior · 2023Article
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
introductionAutoimmune encephalitis (AE) is caused by autoantibodies attacking neuronal cell surface antigens and/or synaptic antigens. We previously demonstrated that S100A6 was hypomethylated in patients with AE and that it promoted B lymphocyte infiltration through the simulated blood-brain barrier (BBB). In this study, we focused on the epigenetic regulation of S100A6, the process by which S100A6 affects B lymphocyte infiltration, and the therapeutic potential of S100A6 antibodies.
methodsWe enrolled and collected serum from 10 patients with AE and 10 healthy control (HC) subjects. Promoter methylation and 5-azacytidine treatment assays were conducted to observe the methylation process of S100A6. The effect of S100A6 on B lymphocytes was analyzed using an adhesion assay and leukocyte transendothelial migration (LTEM) assay. A LTEM assay was also used to compare the effects of the serum of HCs, serum of AE patients, S100A6 recombinant protein, and S100A6 antibodies on B lymphocytes.
resultThe promoter methylation and 5-azacytidine treatment assays confirmed that S100A6 was regulated by DNA methylation. The adhesion study demonstrated that the addition of S100A6 enhanced adhesion between B lymphocytes and a BBB endothelial cell line in a concentration-dependent manner. The LTEM assay showed that the serum of AE patients, as well as S100A6, promoted B lymphocyte infiltration and that this effect could be attenuated by S100A6 antibodies.
conclusionWe clarified that S100A6 was under epigenetic regulation in patients with AE and that it helped B lymphocytes to adhere to and infiltrate the BBB endothelial layer, which could be counteracted by S100A6 antibodies. Therefore, the methylation profile of S100A6 could be a marker of the activity of AE, and countering the effect of S100A6 may be a potential treatment target for AE.
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