NF-κB and innate immunity in ischemic stroke

Ann N Y Acad Sci. 2010 Oct;1207:32-40. doi: 10.1111/j.1749-6632.2010.05735.x.


Acute cerebral ischemia elicits an innate immune response that leads to a cascade of events that culminates in necrotic death of neurons and injury to their supportive structures in the neurovascular unit. Indeed, clinical studies have shown a close relationship between elevated levels of inflammatory markers and the risk for ischemic stroke. However, the signaling pathways that link these events are not well understood. A central regulator of inflammatory response is the transcription factor, nuclear factor-kappa B (NF-κB). The activation of NF-κB is required for the transcriptional induction of many proinflammatory mediators involved in innate immunity, such as cellular adhesion molecules, cytokines, and growth factors. Therefore, factors that modulate the activity of NF-κB could potentially regulate inflammatory processes in ischemic stroke. Here, we review the relationship between NF-κB and ischemic stroke, its role in the neurovascular unit, and discuss some animal models that suggest that this relationship is causal.

Publication types

  • Review

MeSH terms

  • Animals
  • Brain Ischemia / immunology*
  • Disease Models, Animal
  • Humans
  • Immunity, Innate*
  • Inflammation / etiology
  • Inflammation / genetics
  • Inflammation / immunology
  • Models, Neurological
  • NF-kappa B / immunology*
  • Neuroimmunomodulation / immunology
  • Stroke / immunology*
  • Transcriptional Activation


  • NF-kappa B