An amino-terminal-modified methionylated form of CCL5 (Met-RANTES) antagonized the binding of CCL3 and CCL5 to their receptors CCR1 and CCR5, respectively, and the blockade inhibited arthritis in AIA rats via the suppression of neutrophil and macrophage migration into the joints (164). This evidence concerns the gene CCL3 and arthritic joint disease.