Antibody-mediated blockade of CCL2 in Il17g/gIl1rn−/− mice reduced infiltration of CCR2+ GFP+ γδ T cells in joints and suppressed the development of arthritis, suggesting that CCR2+ γδ17 cell accumulation in the joints, which is critical for the development of arthritis, is mediated by the CCL2–CCR2 interaction. This evidence concerns the gene CCR2 and arthritic joint disease.