Epileptic encephalitis: The role of the innate and adaptive immune system

Jan Bauer, Annamaria Vezzani, Christian G. Bien

Research output: Contribution to journalArticlepeer-review


Seizures are a prominent clinical feature of encephalitis. Recent data suggest the adaptive as well as innate immune system to be involved directly in the pathomechanism of epileptogenesis. Cytotoxic T-cells and antibody-mediated complement activation are major components of the adaptive immune system, which can induce neurodegeneration, thereby probably contributing to epileptic encephalitis. The innate immune system operates via interleukin-1 and toll-like receptor-associated mechanisms and was shown to play a direct role in epileptogenesis. Here, we review neuropathology hallmarks of various encephalitis conditions such as Rasmussen encephalitis (RE) but also introduce the more recently discovered antibody-associated voltage-gated potassium channel complex (VGKC), N-methyl-D-aspartate receptor (NMDAR) or glutamic acid decarboxylase (GAD) 65 encephalitides. Neuropathological investigations are used to determine specific cellular components and molecular mechanisms used by the immune system to provoke neurodegeneration and to promote epileptogenesis. Based on recent findings, we propose concepts for the stratification of epileptic encephalitis. Knowledge of the role of the innate immunity has already translated into clinical treatment strategies and may help to discover novel drug targets for these epileptic disorders.

Original languageEnglish
Pages (from-to)412-421
Number of pages10
JournalBrain Pathology
Issue number3
Publication statusPublished - May 2012


  • Antibodies
  • Brain
  • Cytotoxic T-cells
  • Encephalitis
  • Interleukin-1
  • Microglial cells
  • Neuropathology
  • Seizures
  • Toll-like receptors

ASJC Scopus subject areas

  • Neuroscience(all)
  • Pathology and Forensic Medicine
  • Clinical Neurology


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