Flow cytometric analysis of CD58 expression on human PBMCs (human peripheral blood mononuclear cells). Human PBMCs were stained with either FITC Rabbit IgG Isotype Control (left panel) or SDT FITC Rabbit Anti-Human CD58 Antibody (right panel) at 5 ul/test. Flow cytometry and data analysis were performed using BD FACSymphony™ A1 and FlowJo™ software.
Product Details
Product Details
Product Specification
| Host | Rabbit |
| Antigen | CD58 |
| Synonyms | Lymphocyte function-associated antigen 3; LFA3 |
| Immunogen | Recombinant Protein |
| Location | Cell membrane |
| Accession | P19256 |
| Clone Number | S-1046-14 |
| Antibody Type | Recombinant mAb |
| Isotype | IgG |
| Isotype Control | S0B8556 |
| Application | FCM |
| Reactivity | Hu |
| Positive Sample | Human PBMC |
| Purification | Protein A |
| Concentration | 0.2 mg/ml |
| Conjugation | FITC |
| Physical Appearance | Liquid |
| Storage Buffer | PBS, 1% BSA, 0.09% sodium azide |
| 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
CD58, also known as lymphocyte function-associated antigen 3 (LFA-3), is a widely expressed glycosylphosphatidylinositol (GPI)-anchored or transmembrane cell adhesion molecule belonging to the immunoglobulin superfamily that serves as the primary ligand for CD2 on T cells and natural killer (NK) cells. Located on chromosome 1p13 in humans, this protein plays a pivotal role in immune regulation by mediating antigen-independent cell-cell adhesion and providing essential costimulatory signals that lower the threshold for T-cell receptor activation, thereby facilitating T-cell proliferation, cytokine production, and cytolytic activity during immune synapse formation. Beyond its physiological functions in adaptive immunity, CD58 is clinically significant as its expression is frequently downregulated or lost in various malignancies, including diffuse large B-cell lymphoma and acute myeloid leukemia, serving as a mechanism of immune evasion, while conversely, its interaction with CD2 has been exploited therapeutically through agents like alefacept to modulate T-cell responses in autoimmune diseases such as psoriasis.
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