CCR6 and arthritic joint disease: Similar results with respect to lymphocyte migration have been obtained in the SKG mouse model of spontaneous experimental arthritis in which a preferential recruitment of Th17 cells to inflamed, CCL20-expressing, synovial joints was observed that could be inhibited with a neutralizing anti-CCR6 antibody [18], whereas polymorphisms in the CCR6 gene were reported to be associated with rheumatoid arthritis susceptibility [19, 20].