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Fig. 2 | Journal of Neuroinflammation

Fig. 2

From: High levels of endothelial ICAM-1 prohibit natalizumab mediated abrogation of CD4+ T cell arrest on the inflamed BBB under flow in vitro

Fig. 2

NTZ reduces T cell adhesion to immobilized recombinant VCAM-1 in a dose dependent manner. Number of human CD4+ Th1 cells adhering to immobilized recombinant VCAM-1 under static conditions. Th1 cells were pre-treated with titrated concentrations of natalizumab (NTZ) (A), bNTZ (B) and mNTZ (C) as indicated. An isotype control antibody was used as internal control (1 μg/mL Ctrl). Immobilized recombinant DNER was used as negative control (Neg Ctrl). Statistically significant differences are shown only for the comparison with the Ctrl condition. Number of adhered human Th1 (D), Th1* (E), Th2 (F) and Th17 cells (G) on immobilized recombinant VCAM-1 under static conditions. Th1* cells were treated with the minimal significant inhibitory concentration of NTZ (0.01 μg/mL), bNTZ (0.01 μg/mL) and mNTZ (0.1 μg/mL) found in the prior experiment (A–C). An isotype control antibody was used as internal control (0.01 or 0.1 μg/mL Ctrl). A–G Each figure shows the mean ± SEM of 3 independent experiments. Statistical analysis: one-way ANOVA followed by Tukey’s multiple-comparison test (p < 0.05 = *, p < 0.01 = **, p < 0.001 = ***, p < 0.0001 = ****). H Multicolor flow cytometry analysis for α4 -, β1- and β7-integrin cell-surface expression on human Th1 (green), Th1* (red), Th2 (blue) and Th17 cells (orange). Histogram plots are representative for 3 individual experiments

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