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Curr Allergy Asthma Rep. 2003 Jan;3(1):86-93.

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

Author information

1
Department of Neurology, Microbiology and Immunology and the Cancer Center, University of Rochester, 601 Elmwood Avenue, Box 605, Rochester, NY 14642, USA. benjamin_segal@urmc.rochester.edu

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.

PMID:
12543000
[Indexed for MEDLINE]

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