Modur V, Li Y, Zimmerman G A, Prescott S M, McIntyre T M
Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, Utah 84112, USA.
J Clin Invest. 1997 Dec 1;100(11):2752-6. doi: 10.1172/JCI119821.
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-6Ralpha), 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-6Ralpha 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.
内皮细胞通过募集和激活白细胞来启动炎症反应。白细胞介素-6(IL-6)并非此过程的激动剂,但我们发现,可溶性IL-6受体α亚基(IL-6Rα)及其组成性IL-6合成,刺激内皮细胞合成E-选择素、细胞间黏附分子-1、血管细胞黏附分子-1、IL-6和IL-8,并结合中性粒细胞。中性粒细胞表达大量IL-6Rα,并在受到刺激时将其释放:该物质通过新形成的IL-6受体激活内皮细胞。从血管外间隙被激活的多形核中性粒细胞(PMN)向周围内皮细胞的逆行信号传导将募集更多种类的白细胞。限制信号是一种可溶性受体,而非细胞因子。