腺苷 A3 受体刺激可抑制人嗜酸性粒细胞的迁移。
Adenosine A3 receptor stimulation inhibits migration of human eosinophils.
作者信息
Knight D, Zheng X, Rocchini C, Jacobson M, Bai T, Walker B
机构信息
University of British Columbia Pulmonary Research Laboratory, St. Paul's Hospital, Vancouver, Canada.
出版信息
J Leukoc Biol. 1997 Oct;62(4):465-8. doi: 10.1002/jlb.62.4.465.
Activation of adenosine A3 receptors (A3-R) produced a dose-dependent reduction in the chemotaxis of human eosinophils to platelet-activating factor (PAF), RANTES, and leukotriene B4 (LTB4) to a maximum of 58, 48, and 52%, respectively (P < 0.02). This effect was completely reversed by selective A3-R antagonists. In contrast, activation of A1 or A2a-R did not affect PAF-induced eosinophil chemotaxis. PAF up-regulated the expression of CDllb/CD18, down-regulated L-selectin, and also increased F-actin assembly in eosinophils. The expression of these activation markers was not influenced by A3-R, A2a, or A1-R stimulation. Activation of A3-R may play an important role in inflammation by inhibiting eosinophil migration.
腺苷 A3 受体（A3-R）的激活导致人嗜酸性粒细胞对血小板活化因子（PAF）、调节激活正常 T 细胞表达和分泌的趋化因子（RANTES）以及白三烯 B4（LTB4）的趋化作用呈剂量依赖性降低，最大降幅分别为 58%、48%和 52%（P < 0.02）。这种效应被选择性 A3-R 拮抗剂完全逆转。相比之下，A1 或 A2a-R 的激活并不影响 PAF 诱导的嗜酸性粒细胞趋化作用。PAF 上调嗜酸性粒细胞中 CDllb/CD18 的表达，下调 L-选择素，还增加 F-肌动蛋白组装。这些激活标志物的表达不受 A3-R、A2a 或 A1-R 刺激的影响。A3-R 的激活可能通过抑制嗜酸性粒细胞迁移在炎症中发挥重要作用。
Zotero 插件