Bardi Giuseppe, Niggli Verena, Loetscher Pius
Theodor Kocher Institute, P.O. Box, CH-3000 9 Bern, Switzerland.
FEBS Lett. 2003 May 8;542(1-3):79-83. doi: 10.1016/s0014-5793(03)00351-x.
We studied the role of Rho kinase and extracellular signal-regulated kinase (ERK)-2 in the polarization and migration of T lymphocytes in response to the CCR7 ligands EBI1 ligand chemokine (ELC; CCL19) and secondary lymphoid-tissue chemokine (SLC; CCL21). Both Rho kinase protein isoforms are expressed in T lymphocytes. Inhibition of the Rho kinases with Y-27632 strongly inhibited SLC- and ELC-induced polarized morphology and chemotaxis of T lymphocytes. Although the chemokines induced ERK-2 activation, the blockade of this signaling pathway showed no effect on polarization and migration. This study indicates an important role of Rho kinase in CCR7-mediated polarization and migration of T lymphocytes, whereas ERK-2 is not involved in these processes.
我们研究了Rho激酶和细胞外信号调节激酶(ERK)-2在T淋巴细胞响应CCR7配体EBI1配体趋化因子(ELC;CCL19)和次级淋巴组织趋化因子(SLC;CCL21)时的极化和迁移中的作用。两种Rho激酶蛋白亚型均在T淋巴细胞中表达。用Y-27632抑制Rho激酶可强烈抑制SLC和ELC诱导的T淋巴细胞极化形态和趋化作用。尽管趋化因子诱导了ERK-2激活,但阻断该信号通路对极化和迁移没有影响。这项研究表明Rho激酶在CCR7介导的T淋巴细胞极化和迁移中起重要作用,而ERK-2不参与这些过程。