RESUMO
Autoimmune epilepsy (AE) is a type of epilepsy mediated by autoantibodies and immune cells. The main pathogenesis of AE is that autoimmune antibodies related to AE interact with surface of nervous cell membrane antigens or intracellular antigens, which leads to the disorder of excitatory and inhibitory nervous system and causes epileptic seizures. Glutamate receptor subunit 3 peptide B antibodies (GluR3B Ab's) are one type of anti-neuron autoantibodies related to AE, and they can combine with GluR3B subunit of α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid receptor (AMPAR), which causes an increase of intracellular calcium. Intracellular calcium overload further leads to dysregulation of energy metabolism in neurons or oligodendrocyte progenitor cells (OPCs). The damage of neurons or OPCs eventually trigger seizure. Here, we mainly discuss the mechanisms of GluR3B Ab's involving in the development of autoimmune epilepsy.