Flow cytometric analysis of Human CD209 expression on Human peripheral blood monocyte-derived dendritic cells. Human peripheral blood monocyte-derived dendritic cells were stained with FITC Mouse Anti-Human CD11c antibody and either Alexa Fluor® 647 Mouse IgG2a, κ Isotype Control (Left panel) or SDT Alexa Fluor® 647 Mouse Anti-Human CD209 Antibody (Right panel) at 5 μl/test. Flow cytometry and data analysis were performed using BD FACSymphony™ A1 and FlowJo™ software.
Product Details
Product Details
Product Specification
Host | Mouse |
Antigen | CD209 |
Synonyms | CD209 antigen; C-type lectin domain family 4 member L; Dendritic cell-specific ICAM-3-grabbing non-integrin 1 (DC-SIGN; DC-SIGN1); CLEC4L |
Location | Cell membrane |
Accession | Q9NNX6 |
Clone Number | S-2881 |
Antibody Type | Mouse mAb |
Isotype | IgG2a,k |
Application | FCM |
Reactivity | Hu |
Positive Sample | Human peripheral blood monocyte-derived dendritic cells |
Purification | Protein A |
Concentration | 0.2 mg/ml |
Conjugation | Alexa Fluor® 647 |
Physical Appearance | Liquid |
Storage Buffer | PBS, 1% BSA, 0.3% Proclin 300 |
Stability & Storage | 12 months from date of receipt / reconstitution, 2 to 8 °C as supplied |
Dilution
application | dilution | species |
FCM | 5μl per million cells in 100μl volume | Hu |
Background
CD209 (also called DC-SIGN) is a C-type lectin transmembrane receptor encoded by the CD209 gene, expressed predominantly on immature dendritic cells and macrophages; its extracellular carbohydrate-recognition domain binds high-mannose glycans on a broad spectrum of pathogens—ranging from HIV-1, HCV, Ebola, Dengue and SARS-CoV to mycobacteria—thereby functioning as a pattern-recognition receptor that triggers pathogen internalization, lysosomal degradation and subsequent MHC-II-restricted antigen presentation to prime T cells, while also mediating dendritic cell rolling on ICAM-2/ICAM-3 for migration and immune-synapse formation, with polymorphisms in its neck region linked to altered susceptibility to HIV-1 and SARS severity.
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