Region-specific regulation of inflammation and pathogenesis in experimental autoimmune encephalomyelitis

Angela S. Archambault, Julia Sim, Erin E. McCandless, Robyn S. Klein, John H. Russell

Research output: Contribution to journalArticlepeer-review

23 Scopus citations


Experimental autoimmune encephalomyelitis (EAE) is an animal model of multiple sclerosis and is characterized by an infiltrate of predominately T cells and macrophages in the spinal cord and brain. In both the spinal cord and the cerebellum, Th1 cells direct inflammation to antigen-rich white matter tracts, and there is a TNFR1-dependent recruitment of CD11bhi cells in both regions. In the spinal cord, parenchymal invasion, demyelination and clinical symptoms are associated with TNFR1-dependant parenchymal induction (especially astrocytes) of VCAM-1 and CXCL2. None of these events occur in the cerebellum despite the fact that an inflammatory infiltrate accumulates in the perivascular space. Therefore regional specificity in astrocyte responses to inflammatory cytokines may regulate regional parenchymal infiltration and pathogenesis.

Original languageEnglish
Pages (from-to)122-132
Number of pages11
JournalJournal of Neuroimmunology
Issue number1-2
StatePublished - Dec 2006


  • Cerebellum
  • Chemokines
  • Experimental autoimmune encephalomyelitis
  • T cells
  • VCAM-1


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