In this chapter we review the inflammatory mechanisms involved in epileptogenesis, the caveats and limitations of the term autoimmune epilepsy, and two epileptic syndromes of autoimmune origin: epilepsy associated with GAD antibodies and Rasmussen encephalitis. The International League Against Epilepsy (ILAE) recently proposed the definition of acute symptomatic seizures secondary to autoimmune encephalitis for the seizures that occur in the setting of the active phase of immune-mediated encephalitis. In contrast, the term autoimmune epilepsy applies to chronic seizures considered to be secondary to autoimmune brain diseases. If promptly diagnosed and treated, patients with symptomatic seizures due to antibody-mediated encephalitis rarely evolve to develop epilepsy and, therefore, they do not fulfil criteria of autoimmune epilepsy. Scoring systems to predict autoimmune seizures are not very useful because they rely on the presence of additional neurological manifestations or diagnostic tests included in the definition of autoimmune encephalitis. Antibodies against neuronal surface antigens occur in a minority (<5%) of patients with isolated epilepsy; the significance of these antibodies is unclear as the spectrum of symptoms of these patients is not different from that of seronegative cases. In contrast, antibodies against GAD (an intracellular protein) occur in a small subset of patients with temporal lobe epilepsy that is usually refractory to anti-seizure medication.