Experimental autoimmune encephalomyelitis: cytokines, effector T cells, and antigen-presenting cells in a prototypical Th1-mediated autoimmune disease

Curr Allergy Asthma Rep. 2003 Jan;3(1):86-93. doi: 10.1007/s11882-003-0017-6.


Experimental autoimmune encephalomyelitis (EAE) is widely depicted as the prototypical CD4+ Th1-mediated autoimmune disease. Microglia and perivascular macrophages are believed to act as antigen-presenting cells during the effector phase of EAE. In this article, recent data that challenge these conceptions are reviewed. Several recent studies have shown that myelin-reactive CD8+ T cells can mediate inflammatory demyelination. Furthermore, dendritic-like cells have been detected in EAE lesions and implicated in encephalitogenic T-cell activation. Although Th1 polarizing monokines, such as interleukin-12 (IL-12) and possibly IL-23, are critical for the manifestation of EAE, individual Th1 effector cytokines were found to be dispensible.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • Antigen-Presenting Cells / immunology
  • Central Nervous System / immunology
  • Cytokines / immunology
  • Encephalomyelitis, Autoimmune, Experimental / immunology*
  • Humans
  • Syndrome
  • T-Lymphocytes, Regulatory / immunology
  • Th1 Cells / immunology


  • Cytokines