STAT3 signaling is associated with neuroimmune dysregulation in a Dravet syndrome model and pediatric drug-resistant epilepsy

Background: gene mutations. Its core characteristics are heat sensitivity and refractoriness, and immunoinflammatory factors can participate in the occurrence and development of the disease. At present, the regulatory role of immune inflammation activation in DS has been confirmed, but the specific molecular core connecting systemic inflammation and central nervous system signals and its translational relevance to broader pediatric drug-resistant epilepsy (DRE) remains unclear. Methods: mice via qRT-PCR, Western blotting, and immunofluorescence, using robust linear models to confirm central-peripheral inflammation correlations. Results: < 0.001). Conclusion: This study identifies systemic and neuroinflammatory changes in DS associated with increased STAT3 signaling and this inflammatory signature is also observed in the broader pediatric DRE population. By bridging verified molecular mechanisms with real-world clinical data from our pediatric cohort, we suggest peripheral indices (NLR, SII, CRP) that may serve as accessible clinical indicators of disease severity in pediatric DRE. Pending functional validation, these findings identify STAT3 as a pathway of interest and a potential therapeutic candidate, supporting the development of adjunctive anti-inflammatory therapies targeting neuroimmune cascades for DS and broader refractory epilepsies.