Interaction Between Peripheral Cytokines and Central Neuroinflammation in Temporal Lobe Epilepsy

ABSTRACT Purpose Neuroinflammation is a key pathogenic mechanism in temporal lobe epilepsy, quantifiable in vivo using positron emission tomography targeting the translocator protein. This study integrated [ 18 F]DPA‐714 PET/MRI with serum cytokine profiling to investigate this central–peripheral immune relationship in TLE patients. Methods A prospective study of 24 TLE patients and 24 healthy controls (HCs) was conducted. PET/MRI data were available for 24 TLE patients and 7 HCs, while cytokine data were available for all 24 participants in both groups. Standardized uptake value ratios of [ 18 F]DPA‐714 were calculated for key temporal lobe regions. Serum levels of IL‐2, IL‐4, IL‐6, IL‐10, IL‐17, TNF‐α, and IFN‐γ were quantified. Results Compared with HCs, TLE patients demonstrated significantly increased [ 18 F]DPA‐714 PET/MRI uptake in ipsilateral temporal lobe structures (group main effect: F 1,29 = 15.779, p < 0.001), accompanied by a proinflammatory serum profile with elevated IL‐17 and IFN‐γ and decreased IL‐2, IL‐4, and IL‐10 levels ( p < 0.05). Ipsilateral hippocampal [ 18 F]DPA‐714 SUVR was positively correlated with disease duration ( ρ = 0.46, p = 0.025) and seizure frequency ( ρ = 0.52, p = 0.018). However, no significant associations were observed between neuroimaging‐assessed central neuroinflammation and serum cytokines. Conclusion [ 18 F]DPA‐714 PET/MRI precisely demonstrates focal neuroinflammation in TLE patients, correlating with clinical severity, yet the lack of correlation with peripheral markers highlights that peripheral and central immune responses represent distinct and relatively independent inflammatory processes in TLE.