自身免疫性神经炎症中的 T(H)17 细胞因子。
T(H)17 cytokines in autoimmune neuro-inflammation.
机构信息
Institute of Experimental Immunology, University of Zurich, Zurich, Switzerland.
出版信息
Curr Opin Immunol. 2011 Dec;23(6):707-12. doi: 10.1016/j.coi.2011.08.005. Epub 2011 Sep 9.
Abstract
It has been firmly established that IL-23 polarized T(H)17 cells are potent effectors in the pathogenesis of experimental autoimmune encephalitomyelitis (EAE). However, the relative importance of these cells in comparison to other encephalitogenic T(H) subsets, and the mechanisms that they employ to effect inflammatory demyelination, are topics of continuing investigation. Interestingly, deletion of individual 'T(H)17 cytokines', such as IL-17A, IL-17F, IL-22 and IL-21, does not phenocopy the complete EAE-resistance of IL-23-deficient mice. The instability of T(H)17 cells in vivo introduces an additional layer of complexity to their role in the context of relapsing or chronic disease. Recent data indicate that IL-23 drives the production of myeloid activating factors, such as GM-CSF, by myelin-reactive T cells and facilitates their accumulation in the CNS. This review discusses the above issues in relation to the use of T(H)17 cells and related factors as potential therapeutic targets and biomarkers in CNS autoimmune diseases such as multiple sclerosis (MS).
摘要
已经明确的是，IL-23 极化的 T(H)17 细胞是实验性自身免疫性脑脊髓炎（EAE）发病机制中的有效效应物。然而，与其他致脑炎性 T(H)细胞亚群相比，这些细胞的相对重要性，以及它们用于引发炎症性脱髓鞘的机制，仍是正在研究的课题。有趣的是，缺失个别“T(H)17 细胞因子”，如 IL-17A、IL-17F、IL-22 和 IL-21，并不能完全模拟 IL-23 缺陷型小鼠的 EAE 抗性。T(H)17 细胞在体内的不稳定性为其在复发或慢性疾病中的作用增加了一层复杂性。最近的数据表明，IL-23 驱动髓样激活因子，如 GM-CSF，由髓鞘反应性 T 细胞产生，并促进它们在中枢神经系统中的积累。这篇综述讨论了与 T(H)17 细胞和相关因子作为潜在治疗靶点和生物标志物在多发性硬化症（MS）等中枢神经系统自身免疫性疾病中的应用相关的上述问题。
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