Astrocytes stimulate interleukin-17 and interferon-γ production in vitro
Astrocytes stimulate interleukin-17 and interferon-γ production in vitro
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DOI：
10.1002/jnr.21453
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发表时间：
2007-12-01
影响因子：
4.2
通讯作者：
Mostarica-Stojkovic, Marija
中科院分区：
文献类型：
--
作者：
Miljkovic, Djordje;Momcilovic, Mijana;Mostarica-Stojkovic, Marija
星形胶质细胞在中枢神经系统（CNS）炎症过程中，在常驻细胞和浸润细胞之间的复杂相互作用网络中发挥着重要作用，但尚未得到很好的理解。在这样一个复杂的网络中，细胞因子代表了细胞间通讯的重要手段，星形胶质细胞能够影响它们的产生和/或释放。在浸润细胞产生的各种细胞因子中，干扰素(IFN)- γ和白细胞介素(IL)-17是本研究的重点，因为它们分别是辅助性t细胞1型（Th1）和辅助性t细胞17型（Th17）的关键细胞因子。重要的是，Th1和Th17细胞及其细胞因子已被证明在实验性自身免疫性脑脊髓炎（EAE）的发病机制中起重要作用，EAE是一种具有炎症发病机制、多发性硬化症的典型中枢神经系统疾病的动物模型。因此，我们在体外分别研究了星形胶质细胞对健康大鼠和EAE发生大鼠的豆豆蛋白A和髓鞘碱性蛋白刺激的淋巴结细胞中ifn - γ和IL-17生成的影响。星形胶质细胞上调T细胞中IL-17和ifn - γ基因表达和蛋白合成，这与共培养中星形胶质细胞表达IL-23亚基p19和常见IL-12/IL-23亚基p40而不表达IL-12亚基p35的能力一致。这些结果提示了星形胶质细胞在中枢神经系统炎症过程中参与复杂相互作用的另一种方式。(C) 2007 Wiley-Liss, Inc。
Astrocytes play important roles in the complex and as yet not very well understood net of interactions among resident and infiltrating cells during central nervous system (CNS) inflammation. In such an intricate network, cytokines represent an essential means for intercellular communication, and astrocytes are able to affect their generation and/or release. Among various cytokines produced by infiltrating cells, interferon (IFN)-gamma and interleukin (IL)-17 are the focus of this research, because they are pivotal cytokines of helper T-cell type 1 (Th1) and helper T-cell type 17 (Th17), respectively. Importantly, both Th1 and Th17 cells, as well as their cytokines, have been shown to be of importance for the pathogenesis of experimental autoimmune encephalomyelitis (EAE), an animal model of a prototypical CNS disease with inflammatory pathogenesis, multiple sclerosis. Therefore, the influence of astrocytes on the generation of IFN-gamma and IL-17 in concanavalin A- and myelin basic protein-stimulated lymph node cells of healthy rats and rats with developing EAE, respectively, was investigated in vitro. Astrocytes up-regulated IL-17 and IFN-gamma gene expression and protein synthesis in T cells, which coincided with astrocytes' ability to express IL-23 subunit p19 and common IL-12/IL-23 subunit p40 but not IL-12 subunit p35 in the cocultivations. These results suggest one more way in which astrocytes could contribute to the complex interactions during CNS inflammation. (C) 2007 Wiley-Liss, Inc.