Innate immune signalling, neuroinflammation and network plasticity in temporal lobe epilepsy - PubMed
3 hours ago
- #immunotherapy
- #epileptogenesis
- #neuroinflammation
- Temporal lobe epilepsy (TLE) arises from molecular, cellular, and structural disturbances triggered by cerebral insults like convulsive status epilepticus, viral encephalitis, and traumatic brain injury.
- Innate immune pathways (TLR2, TLR3, TLR4, IL-1R1, NLRP3 inflammasome) are central drivers of epileptogenesis, not just secondary effects.
- Immune activation leads to neuroinflammation, altered ion channels, enhanced excitation, impaired inhibition, and synaptic loss, lowering seizure threshold.
- Targeted interventions (TLR4 antagonists, IL-1 inhibitors, NLRP3 inhibitors) reduce seizures and hippocampal atrophy, especially when administered early.
- Some antiseizure medications (e.g., levetiracetam) have immunomodulatory effects, linking immune regulation to seizure control.
- The TLR7-endogenous retrovirus axis may play a role in neuroimmune homeostasis and network instability in TLE.
- Future directions include immune-phenotype stratification, biomarker-guided interventions, and CNS-targeted drug delivery for disease modification.