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. 2018 Oct 26;9:4489. doi: 10.1038/s41467-018-06794-x

Fig. 3.

Fig. 3

CAP228 antibodies efficiently inhibit α4β7 integrin binding. a Inhibition of ConC gp120 binding to α4β7 integrin transfected 293 T cells by V2p mAbs CAP228-16H (green), CAP228-3D (orange) or CH58 (blue). Percentage blocking (y-axis) was calculated from the difference in mean fluorescence intensity (MFI) when cell-gp120 complexes were made in the presence or absence of antibody. The α4β7 specific antibodies HP21 (purple) and ACT1 (red) were used as positive controls, while an irrelevant RSV antibody (palivizumab) and an HIV-1 CD4 binding site-specific antibody (VRC01) were used as the negative controls. b Ability of V2p antibodies CAP228-16H (green) or CH58 (blue) to block adhesion of α4β7 integrin expressing RPMI8866 cells to a cyclic 92TH023 peptide (residues 157–196) at three separate concentrations. c Inhibition of V2 peptide (strains 92TH023 or BG505) binding to α4β7 integrin expressing RPMI8866 cells by V2p mAbs CAP228-16H (green), CAP228-3D (orange), CH58 (blue) and CH59 (light blue) or the conformation specific non-V2p mAb CAP228-9D. The mAb 2B4 is specific for the α4 integrin and served as the positive control (pink). Data are represented as the result of up to three biological replicates used to calculate a mean