Th17 cells in autoimmune demyelinating disease.
Th17 cells in autoimmune demyelinating disease.
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DOI：
10.1007/s00281-009-0186-z
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发表时间：
2010-03
影响因子：
9
通讯作者：
Segal, Benjamin Matthew
中科院分区：
文献类型：
--
作者：
Segal, Benjamin Matthew
关键词：
最近发表的多发性硬化症（MS）和实验性自身免疫性脑脊髓炎（EAE）的研究表明，脱髓鞘斑块的发展与中枢神经系统和外周的Th 17细胞的积累之间的关联。然而，因果关系很难建立。事实上，在迄今为止发表的报告中，白细胞介素（IL）-17 A缺乏或体内中和减弱，但不完全消除，EAE。越来越多的证据表明，临床上类似形式的自身免疫性脱髓鞘疾病可以由不同谱系的髓鞘特异性T细胞驱动，这些T细胞对IL-17 A产生具有不同程度的依赖性，以实现其病理作用。虽然这些观察结果对Th 17阻断剂在MS中的潜在治疗效果产生了怀疑，但集体数据表明，外周血单核细胞中的IL-17 A表达可作为神经炎症和斑块形成的替代生物标志物，并可作为未来临床试验的有用结果指标。
Recently published studies in multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE) have demonstrated an association between the development of demyelinating plaques and the accumulation of Th17 cells in the central nervous system and periphery. However, a causal relationship has been difficult to establish. In fact, in reports published thus far, interleukin (IL)-17A deficiency or neutralization in vivo attenuates, but does not completely abrogate, EAE. There is growing evidence that clinically similar forms of autoimmune demyelinating disease can be driven by myelin-specific T cells of distinct lineages with different degrees of dependence on IL-17A production to achieve their pathological effects. While such observations cast doubts about the potential therapeutic efficacy of Th17 blocking agents in MS, the collective data suggest that IL-17A expression in peripheral blood mononuclear cells could serve as a surrogate biomarker of neuroinflammation and plaque formation and be a useful outcome measure for future clinical trials.
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