Figure 6.
Figure 6. CXCR3-mediated chemotaxis of activated, primary human T lymphocytes and the effect of inhibitors. The chemotactic activity of activated IL-2–expanded, blood-derived human T cells toward 30 nM CXCL11 was determined by the Transwell migration system. Migration is reduced by pretreatment with PTX, the PLC inhibitor U73122, and high concentrations of the kinase inhibitors wortmannin and LY294002. No significant effects on chemotactic activity were found with the inactive analog of U73122 (U73433) and the MEK inhibitors U0126 and PD98059. Data shown are the average of experiments with T cells from at least 5 different donors, except for the different LY294002 concentrations (n = 4). Chemotaxis is expressed as percentage of cells migrating in comparison to 30 nM CXCL11 (set at 100% for each individual donor). Error bars represent SEM. Asterisks indicate values significantly different from CXCL11-induced chemotaxis without inhibitor (Student t test; **P < .001).

CXCR3-mediated chemotaxis of activated, primary human T lymphocytes and the effect of inhibitors. The chemotactic activity of activated IL-2–expanded, blood-derived human T cells toward 30 nM CXCL11 was determined by the Transwell migration system. Migration is reduced by pretreatment with PTX, the PLC inhibitor U73122, and high concentrations of the kinase inhibitors wortmannin and LY294002. No significant effects on chemotactic activity were found with the inactive analog of U73122 (U73433) and the MEK inhibitors U0126 and PD98059. Data shown are the average of experiments with T cells from at least 5 different donors, except for the different LY294002 concentrations (n = 4). Chemotaxis is expressed as percentage of cells migrating in comparison to 30 nM CXCL11 (set at 100% for each individual donor). Error bars represent SEM. Asterisks indicate values significantly different from CXCL11-induced chemotaxis without inhibitor (Student t test; **P < .001).

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