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首页> 外文期刊>Cell metabolism >Interleukin-17 Drives Interstitial Entrapment of Tissue Lipoproteins in Experimental Psoriasis
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Interleukin-17 Drives Interstitial Entrapment of Tissue Lipoproteins in Experimental Psoriasis

机译：白细胞介素-17在实验性牛皮癣中推动组织脂蛋白的间质夹带

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摘要

Lipoproteins trapped in arteries drive atherosclerosis. Extravascular low-density lipoprotein undergoes receptor uptake, whereas high-density lipoprotein (HDL) interacts with cells to acquire cholesterol and then recirculates to plasma. We developed photoactivatable apoA-I to understand how HDL passage through tissue is regulated. We focused on skin and arteries of healthy mice versus those with psoriasis, which carries cardiovascular risk in man. Our findings suggest that psoriasis-affected skin lesions program interleukin-17-producing T cells in draining lymph nodes to home to distal skin and later to arteries. There, these cells mediate thickening of the collagenous matrix, such that larger molecules including lipoproteins become entrapped. HDL transit was rescued by depleting CD4(+) T cells, neutralizing interleukin-17, or inhibiting lysyl oxidase that crosslinks collagen. Experimental psoriasis also increased vascular stiffness and atherosclerosis via this common pathway. Thus, interleukin-17 can reduce lipoprotein trafficking and increase vascular stiffness by, at least in part, remodeling collagen.
机译：血液蛋白捕获在动脉驱动动脉粥样硬化。血管外低密度脂蛋白经历受体吸收，而高密度脂蛋白（HDL）与细胞相互作用以获得胆固醇，然后再循环到血浆。我们开发了PhotoActivaTable apoa-i，了解HDL通道通过组织的调节方式。我们专注于健康小鼠的皮肤和动脉与牛皮癣的小鼠，携带人类的心血管风险。我们的研究结果表明，牛皮癣受影响的皮肤病变计划白细胞介素-17产生的T细胞在将淋巴结排出到家庭中，以后移动到动脉。在那里，这些细胞介导胶原基质的增厚，使得包括脂蛋白的较大分子被捕获。通过耗尽CD4（+）T细胞，中和白细胞介素-17或抑制交联胶原的溶酶氧化酶来拯救HDL转运。实验性牛皮癣还通过这种常见的途径增加了血管僵硬和动脉粥样硬化。因此，白细胞介素-17可以减少脂蛋白运输，并通过至少部分地改造胶原蛋白来增加血管刚度。

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