Abstract
There has been a significant increase in the number of cytokines known to exist, over the past few years. This has led to a re-examination of the established roles of cytokines, as the functions of newly identified members are characterized. In this review, we describe how the recent discovery and characterization of interleukin (IL) -23 has led to a re-evaluation of the role of interferon (IFN) γ and IFNγ-inducing factors in experimental autoimmune encephalomyelitis (EAE). Recent studies suggest that IFNg-secreting T cells, considered the hallmark of EAE, may not be the major detrimental effector cell, and may even have a regulatory function. The impact of this on current understanding of cytokine networks underlying CNS inflammation in EAE is discussed.
Keywords: interferon gamma, interleukin 23, experimental autoimmune encephalomyelitis
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