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首页> 外文期刊>Journal of Neuroimmunology: Official Bulletin of the Research Committee on Neuroimmunology of the World Federation of Neurology >The TLR7 agonist, imiquimod, increases IFN-beta production and reduces the severity of experimental autoimmune encephalomyelitis.
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The TLR7 agonist, imiquimod, increases IFN-beta production and reduces the severity of experimental autoimmune encephalomyelitis.

机译:TLR7激动剂,咪喹莫特增加了IFN-Beta生产,并降低了实验性自身免疫性脑髓炎的严重程度。

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摘要

Experimental autoimmune encephalomyelitis (EAE) is a well-characterised model of autoimmune inflammatory demyelination. Toll-like receptors (TLRs) recognise microbial components and initiate innate immune responses. We report in this study that TLR7 stimulation by imiquimod, a synthetic analog of ssRNA, suppresses disease severity in a chronic EAE model. Disease suppression is associated with increased IFN-beta production in spleens of mice treated with imiquimod. In vitro experiments on pDCs, which express high levels of TLR7 and are potent producers of IFN-beta, suggest that an amplification loop involving TLR7 and IFNAR is required for the observed effects.
机译:实验性自身免疫性脑肌炎(EAE)是一种具有良好特征的自身免疫炎症脱髓鞘模型。 Toll样受体(TLRS)识别微生物组分并引发天生的免疫应答。 我们在这项研究中报告,通过咪喹莫特(SSRNA合成类似物)的TLR7刺激抑制了慢性EAE模型中的疾病严重程度。 疾病抑制与用氨基铵处理的小鼠脾脏的IFN-β产生增加有关。 对PDC的体外实验,其表达高水平的TLR7并是IFN-Beta的有效生产者,表明观察到的效果需要涉及TLR7和IFNAR的放大回路。

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