Mouse CD25/IL-2R alpha APC-conjugated Antibody Summary
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Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.
Detection of CD25/IL-2 R alpha in Mouse Splenocytes by Flow Cytometry. Mouse splenocytes were stained with Rabbit Anti-Human/Mouse FoxP3 PE-conjugated Monoclonal Antibody (Catalog # IC8214P) and either (A) Rat Anti-Mouse CD25/IL-2 R alpha APC-conjugated Monoclonal Antibody (Catalog # FAB9164A) or (B) Rat IgG1Allophycocyanin Isotype Control (Catalog # IC005A). View our protocol for Staining Membrane-associated Proteins.
Preparation and Storage
- 12 months from date of receipt, 2 to 8 °C as supplied.
Background: CD25/IL-2R alpha
IL-2 receptor alpha (IL-2 R alpha ), also known as CD25, is a 55 kDa type I membrane glycoprotein that belongs to the family of cytokine receptors that utilize the common gamma chain subunit ( gamma c). IL-2 R alpha is primarily expressed on activated T cells and on regulatory T cells (Treg). The mouse IL-2 R alpha cDNA encodes a 268 amino acid (aa) precursor that includes a 21 aa signal peptide, a 215 aa extracellular domain (ECD) with two Sushi domains, a 21 aa transmembrane segment, and an 11 aa cytoplasmic domain. Within the ECD, mouse IL-2 R alpha shares 81% and 58% aa sequence identity with rat and human IL-2 R alpha, respectively. It shares approximately 15% aa sequence identity with IL-4, -7, -9, -15, and -21 receptor subunits that also complex with gamma c. IL-2 R beta (CD122) and gamma c (IL-2 R gamma /CD132) dimerize to form a constitutively expressed intermediate affinity IL-2 receptor. By itself, IL-2 R alpha binds IL-2 with low affinity. It associates with IL-2 R beta and gamma c to generate a ternary high affinity IL-2 receptor complex. A soluble form of IL-2 R alpha can be generated by proteolytic cleavage of the cell surface receptor, rendering the T cell unresponsive to IL-2. Increased serum levels of soluble IL-2 R alpha are found in some cancers and immune disorders. IL-2 R alpha is required for Activation Induced Cell Death (AICD) of naive T cells, a mechanism responsible for deleting autoreactive T cell clones. IL-2 R alpha is also required for the development of CD4+CD25+ Treg which suppress autoreactive CD4+ T cells, thereby contributing to peripheral T cell homeostasis.
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