In contrast to γδ17 cells in Il1rn−/− mice, pathogenic Th17 cells expressing CCR6 are recruited to inflammatory sites, such as joints of SKG mice42 and the central nervous system of an experimental autoimmune encephalomyelitis model43, 44, via the CCR6–CCL20 interaction. Here, IL1RN is linked to experimental autoimmune encephalomyelitis.