Mechanisms regulating regional localization of inflammation during CNS autoimmunity

Immunol Rev. 2012 Jul;248(1):205-15. doi: 10.1111/j.1600-065X.2012.01126.x.

Abstract

Multiple sclerosis (MS) is a disease of the central nervous system (CNS) characterized by inflammatory, demyelinating lesions localized in the brain and spinal cord. Experimental autoimmune encephalomyelitis (EAE) is an animal model of MS that is induced by activating myelin-specific T cells and exhibits immune cell infiltrates in the CNS similar to those seen in MS. Both MS and EAE exhibit disease heterogeneity, reflecting variations in clinical course and localization of lesions within the CNS. Collectively, the differences seen in MS and EAE suggest that the brain and spinal cord function as unique microenvironments that respond differently to infiltrating immune cells. This review addresses the roles of the cytokines interferon-γ and interleukin-17 in determining the localization of inflammation to the brain or spinal cord in EAE.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Animals
  • Autoimmunity*
  • Brain / immunology
  • Brain / pathology
  • CD4-Positive T-Lymphocytes / immunology
  • Cellular Microenvironment
  • Central Nervous System / immunology*
  • Cytokines / immunology
  • Encephalomyelitis, Autoimmune, Experimental / immunology*
  • Humans
  • Inflammation / immunology*
  • Multiple Sclerosis / immunology
  • Multiple Sclerosis / pathology
  • Signal Transduction
  • Spinal Cord / immunology
  • Spinal Cord / pathology
  • Th1 Cells / immunology
  • Th17 Cells / immunology

Substances

  • Cytokines