Rap1a and PI3Kγ in neutrophils cooperate to mediate chemokine-triggered, but not selectin-triggered, slow rolling and chemokine-triggered arrest. (A,C) Rolling velocities of neutrophils of the indicated genotype on E-selectin or P-selectin with or without co-immobilized ICAM-1 in the presence or absence of anti-ICAM-1 mAb. (B,D) Percentages of neutrophils of the indicated genotype rolling, arrested and round, or arrested and spread on co-immobilized E-selectin or P-selectin, ICAM-1, and CXCL1. (E-G) Velocities of differentially labeled bone marrow leukocytes from mice of the indicated genotype rolling in TNF-stimulated venules of cremaster muscle, measured before and after injecting a blocking mAb to P-selectin and then a blocking mAb to β2 integrins. The labeled leukocytes were pretreated with PTx and then injected into TNF-challenged WT mice that were previously injected with PTx. (H-J) Numbers of differentially labeled adherent bone marrow leukocytes from the indicated genotype in TNF-stimulated venules of cremaster muscle. The labeled bone marrow leukocytes were injected into TNF-challenged WT mice. The data represent the mean ± SEM from 5 experiments, with 5 mice in each experimental group. *P < .05 for rolling velocity; #P < .05 for percentage of rolling cells compared with that in WT, as determined by unpaired Student t test.