Figure 3
Figure 3. Roles of β2-integrins in anti-MPO–induced glomerular leukocyte adhesion in LPS-pretreated mice. (A) Mice underwent treatment with LPS (0.1 μg, 4 hour) and received either anti–β2-integrin (2E6, 2 mg/kg) or control hamster IgG immediately prior to anti-MPO (50 μg, intravenously) (n = 5/gp). (*P < .001 vs control IgG at the corresponding time points.) (B) Using a similar approach, mice were treated with mAbs against either LFA-1 (M17/4, 170 μg, n = 6) or Mac-1 (5C6, 100 μg, n = 6) to identify which β2-integrin was mediating anti-MPO–induced adhesion. Data were compared with mice treated with isotype control mAb (n = 6). (*P < .001 vs isotype control IgG at same time point, via 2-way ANOVA.)

Roles of β2-integrins in anti-MPO–induced glomerular leukocyte adhesion in LPS-pretreated mice. (A) Mice underwent treatment with LPS (0.1 μg, 4 hour) and received either anti–β2-integrin (2E6, 2 mg/kg) or control hamster IgG immediately prior to anti-MPO (50 μg, intravenously) (n = 5/gp). (*P < .001 vs control IgG at the corresponding time points.) (B) Using a similar approach, mice were treated with mAbs against either LFA-1 (M17/4, 170 μg, n = 6) or Mac-1 (5C6, 100 μg, n = 6) to identify which β2-integrin was mediating anti-MPO–induced adhesion. Data were compared with mice treated with isotype control mAb (n = 6). (*P < .001 vs isotype control IgG at same time point, via 2-way ANOVA.)

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