Nelson, R.Boyd, J.Gladue, R.Paradis, T.Thomas, R.Cunningham, A.Lira, P.Brissette, W.Hayes, L.Hames, L.Neote, K.McColl, S.2007-05-112007-05-112001Genomics, 2001; 73(1):28-370888-75431089-8646http://hdl.handle.net/2440/28063Copyright © 2001 Academic Press. All rights reserved.We describe the genomic organization of a recently identified CC chemokine, MIP3α/CCL20 (HGMW-approved symbol SCYA20). The MIP-3α/CCL20 gene was cloned and sequenced, revealing a four exon, three intron structure, and was localized by FISH analysis to 2q35–q36. Two distinct cDNAs were identified, encoding two forms of MIP-3α/CCL20, Ala MIP-3α/CCL20 and Ser MIP-3α/CCL20, that differ by one amino acid at the predicted signal peptide cleavage site. Examination of the sequence around the boundary of intron 1 and exon 2 showed that use of alternative splice acceptor sites could give rise to Ala MIP-3α/CCL20 or Ser MIP-3α/CCL20. Both forms of MIP-3α/CCL20 were chemically synthesized and tested for biological activity. Both flu antigen plus IL-2-activated CD4+ and CD8+ T lymphoblasts and cord blood-derived dendritic cells responded to Ser and Ala MIP-3α/CCL20. T lymphocytes exposed only to IL-2 responded inconsistently, while no response was detected in naive T lymphocytes, monocytes, or neutrophils. The biological activity of Ser MIP-3α/CCL20 and Ala MIP-3α/CCL20 and the tissue-specific preference of different splice acceptor sites are not yet known.enT-LymphocytesChromosomes, Human, Pair 2HumansCalciumReceptors, ChemokineDNAChemokines, CCMacrophage Inflammatory ProteinsIn Situ Hybridization, FluorescenceChromosome MappingCloning, MolecularAlternative SplicingBase SequenceIntronsExonsMolecular Sequence DataReceptors, CCR6Chemokine CCL20Journal article002001063910.1006/geno.2001.64820001683171000042-s2.0-003530737361899McColl, S. [0000-0003-0949-4660]