Interleukin-1 and neuronal injury: Mechanisms, modification, and therapeutic potential

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Interleukin-1 (IL-1) expression in the brain increases in response to acute and chronic insults, and IL-1 contributes directly to experimentally induced ischaemic, excitotoxic, and traumatic brain injury. Release and cleavage of active IL-1β may be achieved via purinergic P2X7 receptors and activation of caspase-1. The mechanisms of action of IL-1 are largely unknown, but may involve effects on glia, endothelia, and neurones, or on physical parameters within the brain such as temperature or acidity. The naturally occurring IL-1 receptor antagonist (IL-1ra) is currently being considered for treatment of stroke and other disorders. © 2003 Elsevier Science (USA). All rights reserved.
Original languageEnglish
Pages (from-to)152-157
Number of pages5
JournalBrain, Behavior, and Immunity
Issue number3
Publication statusPublished - Jun 2003


  • Interleukin-1
  • Mechanisms
  • Neuronal injury
  • Receptors
  • Stroke
  • Therapeutics


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