Rat CCL20 was initially identified in ischemic brain tissue and called ST38. In experimental autoimmune panencephalomyelitis, CCL20 expression correlates with the onset of inflammation. In experimental autoimmune encephalomyelitis (EAE), CCL20 and CCR6 mRNAs are induced in the CNS of SJL mice; CCL20 is expressed mainly by CNS-infiltrating leukocytes, and it can be expressed by astrocytes as an additional source of CCL20 during disease relapses. CCL20 is involved in the recruitment of leukocytes to sites of injury and inflammation. CCL20 is constitutively expressed in liver, lung, and mucosal epithelial cells (small intestine and colon).? CCL20 is expressed at a low basal level, but its expression is amplified by proinflammatory cytokines and toll-like receptor (TLR) agonists. During infections, CCL20 expression is stimulated in epithelial cells, and immature CCR6+ dendritc cells (DCs) are recruited. Thereafter, the CCR6 expression is downregulated during 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 β-defensin-1 and -2, small cationic antimicrobial peptides, bind and activate CCR6. Contrarily, these β-defensins have lower affinities for CCR6 than CCL20.?
Size
10 μg
Concentration
n/a
Applications
BA
Other Names
Macrophage inflammatory protein-3α (MIP-3 alpha), Liver and activation-regulated chemokine (LARC), Exodus, and ST38, MIP3a, MIP3 alpha, MIP 3 alpha