Journal
CURRENT ALLERGY AND ASTHMA REPORTS
Volume 3, Issue 1, Pages 86-93Publisher
CURRENT SCIENCE INC
DOI: 10.1007/s11882-003-0017-6
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Funding
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS041562] Funding Source: NIH RePORTER
- NINDS NIH HHS [NS41562] Funding Source: Medline
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Experimental autoimmune encephalomyelitis (EAE) is widely depicted as the prototypical CD4+ ThI-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 Thl polarizing monokines, such as interleukin-12 (IL-12) and possibly IL-23, are critical for the manifestation of EAE, individual Thl effector cytokines were found to be dispensible.
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