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Fig. 6 | Journal of Neuroinflammation

Fig. 6

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. 6

Dose dependent inhibition of shear resistant T cell arrest to VCAM-1 is abrogated in the presence of high levels of ICAM-1. Number of arrested human CD4+ Th1* cells on immobilized recombinant VCAM-1 (1X, 1.54 μg/mL) (A, B), and equimolar concentrations of VCAM-1 (1X) / ICAM-1 (1X, 1.14 μg/mL) combined (C, D) under flow conditions. Th1* cells were treated with titrated concentrations of the different natalizumab constructs as indicated (bNTZ: A, C; mNTZ: B, D) and/or with 1 μg/mL of a function blocking anti-β2-integrin antibody (C, D) prior experiment. An isotype control antibody was used as internal control (1 μg/mL Ctrl). E Number of arrested human Th1* cells on equimolar concentration of immobilized recombinant VCAM-1 (1X) and ICAM-1 (1X), and VCAM-1 (1X) / ICAM-1 (1-10X, 1.14–11.4 μg/mL) combined under flow condition. Th1* cells arresting to immobilized recombinant VCAM-1/ICAM-1 combined were treated with 1 μg/mL bNTZ prior experiment. A–E Each figure shows mean ± SEM of 3 independent experiments. Statistical analysis: unpaired T-test (p < 0.05 = *, p < 0.01 = **, p < 0.001 = ***, p < 0.0001 = ****). Significant differences are shown only for the comparison with Ctrl condition

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