• Medientyp: E-Artikel
  • Titel: Activation of innate immunity in the CNS triggers neurodegeneration through a Toll-like receptor 4-dependent pathway
  • Beteiligte: Lehnardt, Seija; Massillon, Leon; Follett, Pamela; Jensen, Frances E.; Ratan, Rajiv; Rosenberg, Paul A.; Volpe, Joseph J.; Vartanian, Timothy
  • Erschienen: Proceedings of the National Academy of Sciences, 2003
  • Erschienen in: Proceedings of the National Academy of Sciences
  • Sprache: Englisch
  • DOI: 10.1073/pnas.1432609100
  • ISSN: 0027-8424; 1091-6490
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  • Beschreibung: <jats:p>Innate immunity is an evolutionarily ancient system that provides organisms with immediately available defense mechanisms through recognition of pathogen-associated molecular patterns. We show that in the CNS, specific activation of innate immunity through a Toll-like receptor 4 (TLR4)-dependent pathway leads to neurodegeneration. We identify microglia as the major lipopolysaccharide (LPS)-responsive cell in the CNS. TLR4 activation leads to extensive neuronal death<jats:italic>in vitro</jats:italic>that depends on the presence of microglia. LPS leads to dramatic neuronal loss in cultures prepared from wild-type mice but does not induce neuronal injury in CNS cultures derived from<jats:italic>tlr4</jats:italic>mutant mice. In an<jats:italic>in vivo</jats:italic>model of neurodegeneration, stimulating the innate immune response with LPS converts a subthreshold hypoxic-ischemic insult from no discernable neuronal injury to severe axonal and neuronal loss. In contrast, animals bearing a loss-of-function mutation in the<jats:italic>tlr4</jats:italic>gene are resistant to neuronal injury in the same model. The present study demonstrates a mechanistic link among innate immunity, TLRs, and neurodegeneration.</jats:p>
  • Zugangsstatus: Freier Zugang