Compared to WT animals, CCR6−/− mice developed less clinical signs of arthritis in the collagen‐induced arthritis model but not in the K/BxN serum transfer arthritis model and in the human tumour necrosis factor transgenic arthritis model, suggesting a defect in adaptive effector functions but intact innate effector functions in the development of arthritis in CCR6−/− animals. This evidence concerns the gene CCR6 and arthritic joint disease.