Retrograde inflammatory signaling from neutrophils to endothelial cells by soluble interleukin-6 receptor alpha
Retrograde inflammatory signaling from neutrophils to endothelial cells by soluble interleukin-6 receptor alpha
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DOI：
10.1172/jci119821
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发表时间：
1997-12-01
影响因子：
15.9
通讯作者：
McIntyre, TM
中科院分区：
文献类型：
--
作者：
Modur, V;Li, YJ;McIntyre, TM
内皮细胞通过募集和激活白细胞来启动炎症反应，IL-6对此不是激动剂，但我们发现可溶性IL-6受体α亚单位（IL-6 R α）与其组成性IL-6合成一起刺激内皮细胞合成E-选择素、细胞内粘附分子-1、血管细胞粘附分子-1、IL-6和IL-8，并结合嗜中性粒细胞，中性粒细胞表达大量的IL-6 R α，并在刺激后脱落：这种物质通过新构建的IL-6受体激活内皮细胞，从血管外隔室中激活的PMN到周围内皮细胞的逆行信号传导将募集更多和更广泛的白细胞。限制信号是可溶性受体，而不是细胞因子。
Endothelial cells initiate the inflammatory response by recruiting and activating leukocytes, IL-6 is not an agonist for this, but we found soluble IL-6 receptor alpha-subunit (IL-6R alpha), with their constitutive IL-6 synthesis, stimulated endothelial cells to synthesize E-selectin, intracellular adhesion molecule-1, vascular cellular adhesion molecule-1, IL-6, and IL-8, and to bind neutrophils, Neutrophils express significant amounts of IL-6R alpha and upon stimulation shed it: this material activates endothelial cells through a newly constituted IL-6 receptor, Retrograde signaling from PMN activated in the extravascular compartment to surrounding endothelial cells will recruit more and a wider variety of leukocytes. The limiting signal is a soluble receptor, not a cytokine.