MIP3 alpha / CCL20 Mouse Monoclonal Antibody [Clone ID: 319F6.07]
MIP3 alpha / CCL20 mouse monoclonal antibody, clone 319F6.07
|Applications||ELISA, FN, IHC|
|Recommended Dilution||DDX0430P-50 / DDX0430P-100 Purified: Blocking migration, ELISA capture, IHC|
|Immunogen||Human recombinant MIP3α in eukaryotic cells.|
Species cross-reactivity: Macaque.
|Formulation||Purified: 100 μg in 200μl /50 μg in 100 μl Tris-NaCl pH 8
|Purification||QMA Hyper D ion exchange chromatography|
|Storage||-20°C. KEEP CONTENTS STERILE: no preservative.
Purified antibodies: avoid repeated freeze/thaw cycles.
Coupled antibodies: glycerol protects from freezing.
|Background||Macrophage inflammatory protein (MIP)-3α/ CCL20 is a CC-type chemokine mapped to chromosome 2 in humans. Langerhans cells (LCs) represent a unique population of DCs colonizing epithelium. MIP-3α plays a central role in LC precursor recruitment into the epithelium during inflammation. (a) Among DC populations, MIP-3α is the most potent chemokine inducing the selective migration of in vitro-generated CD34+ hematopoietic progenitor cell-derived LC precursors and skin LCs in accordance with the restricted MIP-3α receptor (CC chemokine receptor 6) expression by these cells. (b) MIP-3α is mainly produced by epithelial cells, and the migration of LC precursors induced by the supernatant of activated skin keratinocytes is blocked with an antibody against MIP-3α. (c) In vivo, MIP-3α is selectively produced at sites of inflammation as illustrated in tonsils and lesional psoriatic skin where MIP-3α upregulation appears associated with an increase in LC turnover. (d) The secretion of MIP-3α is strongly upregulated by cells of epithelial origin after inflammatory stimuli (interleukin 1β plus TNFα) or T cell signals. (Dieu-Nosjean et al, J;Exp.med, 2000 192: 705-18).|
|Synonyms||CCL20, LARC, MIP3A, MIP-3 alpha, C-C motif chemokine 20, Small-inducible cytokine A20, SCYA20, Exodus-1, Dendritic Cell Marker, DC marker|