Caspase-11 mediates oligodendrocyte cell death and pathogenesis of autoimmune-mediated demyelination

S. Hisahara, J. Yuan, T. Momoi, H. Okano, M. Miura

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115 Citations (Scopus)


Multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE), are inflammatory diseases of the central nervous system (CNS) characterized by localized areas of demyelination. The mechanisms underlying oligodendrocyte (OLG) injury in MS and EAE remain unknown. Here we show that caspase-11 plays crucial roles in OLG death and pathogenesis in EAE. Caspase-11 and activated caspase-3 were both expressed in OLGs in spinal cord EAE lesions. OLGs from caspase-11-deficient mice were highly resistant to the cell death induced by cytotoxic cytokines. EAE susceptibility and cytokine concentrations in the CNS were significantly reduced in caspase-11-deficient mice. Our findings suggest that OLG death is mediated by a pathway that involves caspases-11 and -3 and leads to the demyelination observed in EAE.

Original languageEnglish
Pages (from-to)111-122
Number of pages12
JournalJournal of Experimental Medicine
Issue number1
Publication statusPublished - 2001 Jan 1
Externally publishedYes


  • Apoptosis
  • Cytokines
  • Experimental autoimmune encephalomyelitis
  • Knockout mouse
  • Multiple sclerosis

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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