During infections, CCL20 expression is stimulated in epithelial cells, and immature CCR6+ DC are recruited. Thereafter, CCR6 is downregulated during dendritic cell (DC) maturation, and these migrate to the lymphoid node under the expression of CCR7. CCL20 is the only ligand for CCR6. Nevertheless, mouse and human beta-defensin-1 and -2, small cationic antimicrobial peptides, bind and activate CCR6. Contrarily, these beta-defensins have lower affinities for CCR6 than CCL20. Also, human CCL20 has potent antimicrobial activity. CCL20 and CCR6 play an important role in the pathogenesis of encephalomyelitis and psoriasis (chronic inflammatory skin disorder) in animal models. CCL20 is a chemokine abundant in psoriatic plaques characterized by epidermal hyperproliferation and immunocyte infiltration. CCL20 production from keratinocytes could be an initial trigger for Th17 activation and a key component in maintaining the self-perpetuating cycle of Th17 activation in psoriasis.