Mig requires CCR3 expression for inhibitory activity. (A) The dose-dependent binding of Mig to the surface of wild-type (♦) and CCR3-deficient (▪) cells is shown. Data represent mean ± SD percent mean channel fluorescence (chemokine binding) compared with no chemokine for 3 independent experiments combined. Staining with control antibody (dashed lines) is shown. *P < .05. (B) Mig does not inhibit CCR3-deficient eosinophil chemotaxis toward PAF. Cells were allowed to transmigrate following pretreatment with buffer or Mig. Data represent mean ± SD of eosinophils that migrated toward PAF (10 nM). *P < .05. The results are representative of 3 experiments. (C) Mig does not inhibit PAF-induced actin polymerization in CCR3-deficient eosinophils. Wild-type (dashed line) and CCR3-deficient (solid line) eosinophils were treated with PAF (10 nM, ▪), or Mig (200 nM) and PAF (♦) for the indicated period of time. Cells were fixed and stained with NBD-phallacidin. Relative F-actin content is expressed as the ratio of the mean channel fluorescence between eotaxin- and media alone–stimulated cells. A representative experiment is shown (n = 3).