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

Abstract

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.

• Authors: Benjamin M Segal
• Journal: Current allergy and asthma reports (Curr Allergy Asthma Rep) Vol. 3 Issue 1 Pg. 86-93 (Jan 2003) ISSN: 1529-7322 [Print] United States
• PMID: 12543000 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S., Review)

Chemical References

• Cytokines

Topics

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