ArticleBrain, behavior, & immunity - health2026
Exploring the role of PD-1 as a marker in drug-refractory epilepsy and its potential indication for valproic acid treatment.
Article in Brain, behavior, & immunity - health, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: The immune checkpoint pathway PD-1/PD-L, known for its role in immunosuppression via regulatory T cells (Tregs) and inflammatory signaling, is implicated in the neuroinflammation of drug-refractory epilepsy (DRE). Given the emerging importance of immune dysregulation in epilepsy, identifying immune-related biomarkers may improve diagnosis and guide treatment strategies. Objective: This study aimed to evaluate the potential of PD-1 as a diagnostic biomarker in the cerebrospinal fluid (CSF) and plasma and to investigate whether the therapeutic effect of valproic acid (VPA) in intractable status epilepticus (ISE) is mediated through immunomodulation. Methods: A cohort of 74 patients with DRE (46 with partial seizures (PS) and 28 with ISE) and 25 healthy controls was enrolled. PD-1 levels in CSF and plasma were quantified by flow cytometry and ELISA. In a VPA-treatment sub-study of 25 ISE patients, serial samples were analyzed for PD-1 Results: Significantly elevated PD-1 levels were observed in both plasma and CSF of epilepsy patients compared to controls, with the highest levels in the ISE subgroup. IL-10 and IL-6 levels were also elevated in intractable epilepsy (IE) patients compared to controls. Critically, clinical improvement was associated with a reduction in PD-1 Conclusion: These findings identify PD-1 as a promising immune-inflammatory biomarker for DRE and its severe forms. Moreover, they suggest that the efficacy of VPA in ISE is mediated through the modulation of the PD-1 pathway and related cytokines, rather than a direct concentration-dependent pharmacological effect.
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