Figure 4
Figure 4. Activated leukocyte β2 integrins and CD44 are involved in PBMC adhesion to ECs. Inhibition of PBMC adhesion with antibody (A,B) and recombinant protein (C) was performed as described in “Inhibition assays.” For all experiments, PBMC adhesion was activated by epi-treated SS RBCs as indicated. Results are presented as percentage of adherent PBMCs at a shear stress of 1 dyne/cm2. Error bars show SEM of 3 different experiments for panels A and B and SEM of 4 different experiments for panel C. (A) Inhibition of PBMC adhesion was performed by incubation of activated PBMCs washed free of lysed epi-treated SS RBCs with anti-β2 integrin antibody. P3 protein was used as a nonreactive control for both panels A and B. *P < .001 compared with unstimulated PBMCs; **P < .001 compared with activated PBMCs preincubated with P3. (B) Inhibition of PBMC adhesion was performed by incubation of activated PBMCs washed free of lysed epi-treated SS RBCs with anti-CD47, anti-LW, or anti-CD44 antibody. *P < .001 compared with unstimulated PBMCs; **P < .001 compared with activated PBMCs preincubated with P3. (C) Confluent cultures of HUVECs were incubated without recombinant protein or with sLW or sCD44 protein, washed, and then tested for their ability to support adhesion of activated PBMCs washed free of lysed epi-treated SS RBCs. *P < .001 compared with unstimulated PBMCs; **P < .001 compared with PBMCs coincubated with epi-treated SS RBCs.

Activated leukocyte β2 integrins and CD44 are involved in PBMC adhesion to ECs. Inhibition of PBMC adhesion with antibody (A,B) and recombinant protein (C) was performed as described in “Inhibition assays.” For all experiments, PBMC adhesion was activated by epi-treated SS RBCs as indicated. Results are presented as percentage of adherent PBMCs at a shear stress of 1 dyne/cm2. Error bars show SEM of 3 different experiments for panels A and B and SEM of 4 different experiments for panel C. (A) Inhibition of PBMC adhesion was performed by incubation of activated PBMCs washed free of lysed epi-treated SS RBCs with anti-β2 integrin antibody. P3 protein was used as a nonreactive control for both panels A and B. *P < .001 compared with unstimulated PBMCs; **P < .001 compared with activated PBMCs preincubated with P3. (B) Inhibition of PBMC adhesion was performed by incubation of activated PBMCs washed free of lysed epi-treated SS RBCs with anti-CD47, anti-LW, or anti-CD44 antibody. *P < .001 compared with unstimulated PBMCs; **P < .001 compared with activated PBMCs preincubated with P3. (C) Confluent cultures of HUVECs were incubated without recombinant protein or with sLW or sCD44 protein, washed, and then tested for their ability to support adhesion of activated PBMCs washed free of lysed epi-treated SS RBCs. *P < .001 compared with unstimulated PBMCs; **P < .001 compared with PBMCs coincubated with epi-treated SS RBCs.

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