Sodium/Potassium-transporting ATPase Subunit Alpha-3 Antibody is not Present in Patients with Idiopathic Intracranial Hypertension


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KÜÇÜKALİ C. İ., Soylu S., Ulusoy C., TÜZÜN E.

Haseki Tip Bulteni, cilt.63, sa.1, ss.6-11, 2025 (ESCI, Scopus, TRDizin) identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 63 Sayı: 1
  • Basım Tarihi: 2025
  • Doi Numarası: 10.4274/haseki.galenos.2025.29392
  • Dergi Adı: Haseki Tip Bulteni
  • Derginin Tarandığı İndeksler: Emerging Sources Citation Index (ESCI), Scopus, CINAHL, EMBASE, Directory of Open Access Journals, TR DİZİN (ULAKBİM)
  • Sayfa Sayıları: ss.6-11
  • Anahtar Kelimeler: antibody, autoimmunity, Idiopathic intracranial hypertension, sodium/potassium-transporting ATPase
  • Açık Arşiv Koleksiyonu: AVESİS Açık Erişim Koleksiyonu
  • İstanbul Üniversitesi Adresli: Evet

Özet

Aim: Increased cerebrospinal fluid (CSF) oligoclonal band prevalence, elevated cytokine levels, glial antibodies, and positive response to steroids have been described in idiopathic intracranial hypertension (IIH), suggesting autoimmune etiology in this disease. Sodium/ potassium ATPases have been implicated in CSF production. Our objective was to discern unprecedented autoantibodies specific for sodium/potassium-transporting ATPase subunit alpha-3 (ATP1A3) in IIH. Methods: Sera obtained from 31 individuals clinically diagnosed with IIH and 20 healthy control subjects were subjected to indirect immunofluorescence staining using live cultured rat brain neurons and HEK293 cells transfected with ATP1A3 cDNA. Results: Autoantibodies targeting neuronal cell surface antigens were identified in three patients diagnosed with IIH. However, serum samples from IIH patients and healthy controls did not react with ATP1A3-transfected cells. Conclusion: Our results indicate that ATP1A3 antibodies do not have a primary role in IIH pathogenesis. However, we provide preliminary support for the presence of anti-neuronal autoimmunity.