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

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