Adrenergic control of natural killer cell circulation and adhesion
Adrenergic control of natural killer cell circulation and adhesion
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DOI：
10.1006/brbi.1997.0499
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发表时间：
1997-12-01
影响因子：
15.1
通讯作者：
Schmidt, RE
中科院分区：
文献类型：
--
作者：
Benschop, RJ;Schedlowski, M;Schmidt, RE
自然杀伤（NK）细胞循环受肾上腺素能调节。NK细胞究竟是如何释放到血液循环中的还不得而知。在试图确定一些机制，本报告侧重于NK细胞的粘附调节方面。结果表明，只要受体刺激发生，NK细胞和内皮细胞（EC）之间的相互作用就会被β(2)-肾上腺素能受体刺激减少。肾上腺素输注期间，体内可溶性粘附分子（sICAM-1、sE-selectin、sVCAM-1）水平保持不变。体外分析进一步揭示了NK-EC粘附需要Ca2+/Mg2+。阻断研究表明，β (1)(CD29)-和β (2)(CD18)-整合素家族的几个成员参与其中，使NK细胞粘附减少28%至39%。在这些阻断抗体存在的情况下刺激β(2)-肾上腺素受体进一步降低NK粘附，平均降低22%。NK细胞对各种细胞外基质成分的粘附分析表明，NK细胞对纤维连接蛋白的粘附显著，但对层粘连蛋白或胶原I和n的粘附则少得多。在β(2)-肾上腺素受体刺激下，NK细胞对纤维连接蛋白的粘附减少了50%，与纤维连接蛋白上的vla4 / vla5结合位点无关。综上所述，这些结果有助于理解β -肾上腺素能受体刺激对NK细胞循环和粘附的影响。(C) 1997学术出版社。
Natural killer (NK) cell circulation is subject to adrenergic regulation. Exactly how NK cells are released into the circulation is unknown. In an attempt to identify some of the mechanisms, the present report focuses on aspects of adhesion regulation of NK cells. Results demonstrate that interactions between NK and endothelial cells (EC) in vitro can be reduced by beta(2)-adrenoceptor stimulation for as long as the receptor stimulation occurs. The level of soluble adhesion molecules (sICAM-1, sE-selectin, sVCAM-1) in vivo remained unchanged during adrenaline infusion. In vitro analyses further reveal the requirement for Ca2+/Mg2+ in NK-EC adhesion. Blocking studies indicate the involvement of several members of the beta(1)(CD29)- and beta(2)(CD18)-integrin family, reducing NK cell adhesion by 28 to 39%. Stimulation of beta(2)-adrenoceptors in the presence of these blocking antibodies further reduced NK adhesion by an average of 22%. Analysis of NK cell adhesion to various extracellular matrix components demonstrates significant NK cell adhesion to fibronectin but much less to laminin or collagens I and N. NK cell adhesion to fibronectin was reduced by 50% upon beta(2)-adrenoceptor stimulation, independent of the VLA-4/VLA-5 binding site on fibronectin. Together these results contribute to understanding the influences of beta-adrenoceptor stimulation on NK cell circulation and adhesion. (C) 1997 Academic Press.