The inhibition of CCL1-induced chemotaxis of VSMCs by anti-CCR8 is specific. Media, CCL1 (100 ng/mL), CCL3 (MIP-1α; 100 ng/mL), or PDGF-BB (10 ng/mL) was added to the bottom wells of the chemotaxis chamber. VSMCs, in the presence of IgG1, anti-CCR8, or anti-CCR5 (1 μg/mL), were added to the top wells and the chemotaxis assay was performed as detailed in “Materials and methods.” IgG1, the isotypic antibody control, did not inhibit the chemotactic response of human VSMCs to CCL1 (C1), CCL3, or PDGF-BB (*P < .005). Anti-CCR8 completely inhibited CCL1-induced VSMC chemotaxis but had no inhibitory effect on the chemotaxis induced by CCL3 or by PDGF (P < .005). Antibody directed against the CCL3 receptor CCR5 inhibited the chemotactic response of VSMCs to CCL3 but not to either CCL1 (**P < .003) or to PDGF-BB (*P < .005). This study shows that the inhibition of chemotaxis by anti-CCR8 is specific and not due to a hindrance of chemotaxis due to the attachment of an antibody to a cell-surface receptor. Error bars represent SD.