Flow cytometric analysis of Mouse CTLA-4 (CD152) expression on Concanavalin A stimulated C57BL/6 mouse splenocytes. C57BL/6 mouse splenocytes were stimulated 72h with 2.5μg/ml Concanavalin A and then were stained with Brilliant Violet 421™ Rat Anti-Mouse CD3 and either Biotin Mouse IgG2b, k Isotype Control (left panel) or Biotin Mouse Anti-Mouse CTLA-4 (CD152) Antibody (right panel) at 2 μl/test followed by Sav-PE. Flow cytometry and data analysis were performed using Agilent NovoCyte Quanteon and FlowJo™ software.
Product Details
Product Details
Product Specification
| Host | Mouse |
| Antigen | CTLA-4 (CD152) |
| Synonyms | Cytotoxic T-lymphocyte protein 4; Cd152; Ctla4 |
| Location | Cell membrane |
| Accession | P09793 |
| Clone Number | 9D9 |
| Antibody Type | Mouse mAb |
| Isotype Control | S0B5556 |
| Application | FCM |
| Reactivity | Ms |
| Positive Sample | ConA treated with C57BL/6 mouse splenocytes |
| Purification | Protein G |
| Concentration | 0.5 mg/ml |
| Conjugation | Biotin |
| Physical Appearance | Liquid |
| Storage Buffer | PBS pH7.4, 0.09% sodium azide |
| Stability & Storage | 12 months from date of receipt / reconstitution, 2 to 8 °C as supplied |
Dilution
| application | dilution | species |
| FCM | 1μg per million cells in 100μl volume | Ms |
Background
CTLA-4 (cytotoxic T-lymphocyte-associated protein 4, CD152) is an immune checkpoint molecule primarily expressed on the surface of activated T cells and regulatory T cells (Tregs). It belongs to the immunoglobulin superfamily and shares high structural homology with the T-cell costimulatory receptor CD28. Functionally, CTLA-4 binds to B7 molecules (CD80/CD86) on the surface of antigen-presenting cells and competes with CD28 for these ligands with higher affinity, thereby inhibiting T-cell activation, proliferation, and cytokine secretion. This serves as a "brake" on immune responses and is critical for maintaining self-tolerance and preventing excessive inflammatory reactions. In the tumor microenvironment, cancer cells often exploit the CTLA-4 pathway by upregulating its expression to suppress anti-tumor immune responses, achieving immune evasion. Consequently, CTLA-4 has become a major target in cancer immunotherapy, and its blocking agents (e.g., ipilimumab) can relieve T-cell inhibitory signals and reactivate the immune system to attack tumor cells. However, inhibiting the CTLA-4 pathway may also disrupt immune homeostasis, leading to immune-related adverse events (irAEs) such as colitis, dermatitis, and endocrinopathies, thus requiring close monitoring in clinical practice. Additionally, CTLA-4 gene polymorphisms are closely associated with susceptibility to various autoimmune diseases, including rheumatoid arthritis and type 1 diabetes.
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