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阻断介质素-17A的结果是在apolipoprotein E缺乏的小鼠中减少动脉样硬化

Emily Smith¹, Konkal-Matt R Prasad, Matthew Butcher

¹Robert M. Berne Cardiovascular Research Center, University of Virginia, Charlottesville, USA.

|April 7, 2010

概括

产生中白素-17A (IL-17A) 的T细胞促进动脉样硬化. 阻断IL-17A降低了小鼠的斑块负担和炎症,证明了其益风性作用.

科学领域:

免疫学免疫学免疫学
心血管研究研究心血管研究
炎症生物学炎症生物学

背景情况:

在动脉样硬化期间,T细胞对免疫反应至关重要.
干白素-17A (IL-17A) 在动脉动脉生成中的特定作用尚不清楚.
这项研究调查了动脉样硬化易发生的疾病是否会促进产生IL-17A的T细胞,从而加剧动脉样硬化.

研究的目的:

为了确定患有动脉样硬化倾向的疾病是否诱导IL-17A产生T细胞.
阐明IL-17A在动脉样硬化发展中的作用.
研究IL-17A影响动脉动脉生成的机制.

主要方法:

在阿波利波蛋白E缺陷 (Apoe(-/-)) 小鼠中的量化IL-17A和IL-17A表达T细胞.
具有IL-17A(+) T细胞作为T辅助细胞17 (Th17) 和gamma delta(+) T细胞的特征.
给药IL-17受体A阻塞在Apoe-/-) 小鼠和分析动脉样硬化斑块和炎症标志物.

主要成果:

在阿波埃小鼠中,IL-17A水平和IL-17A(+) T细胞在主动脉和脏中升高.
IL-17A阻断降低了动脉样硬化斑块负担,IL-6,G-CSF和CXCL1的表达.
治疗IL-17A增加了大动脉CXCL1的表达和单细胞粘附ex vivo.

结论:

倾向于动脉样硬化的疾病会诱导产生IL-17A的T细胞.
IL-17A通过驱动单细胞/巨细胞向大动脉壁招募来促进动脉样硬化.
IL-17A在动脉动脉发生过程中起到了益动脉动脉的炎症作用.

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