Curr Allergy Asthma Rep 2003 Jan;3(1):86-93
Department of Neurology, Microbiology and Immunology and the Cancer Center, University of Rochester, 601 Elmwood Avenue, Box 605, Rochester, NY 14642, USA.
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.