Emerging evidence suggests that the immune system may signiﬁ cantly contribute to seizures and epilepsy. The kindling and status epilepticus models of epilepsy provide valuable tools with which to study mechanisms underlying epileptogenesis. Epileptogenesis refers to a dynamic process that progressively alters neuronal excitability and causes reorganization of neuronal networks before the ﬁ rst spontaneous seizure occurs. The inﬂ ammatory changes during epileptogenesis include gliosis and activation of microglia, blood–brain barrier damage and an increase in the expression of proinﬂ ammatory cytokines. Several studies have demonstrated that the activation of proinﬂ ammatory pathways inﬂ uences neurotransmitter systems and neuronal excitability, thereby contributing to epileptogenesis. The inﬂ ammatory pathways represent a promising new target for the development of new drugs, that can prevent epileptogenesis. Various pharmacologic studies report inhibition of seizures and blocking the epileptogenesis by using nonsteroidal anti-inﬂ ammatory drugs and immunosuppressants.