Human CD25/IL-2R alpha Antibody Summary
Accession # P01589
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Cell Proliferation Induced by IL‑2 and Neutralization by Human CD25/IL‑2 R alpha Antibody. Recombinant Human IL-2 (202-IL) stimulates proliferation in the N1186 human T cell line in a dose-dependent manner (orange line). Proliferation elicited by Recombinant Human IL-2 (1 ng/mL) is neutralized (green line) by increasing concentrations of Mouse Anti-Human CD25/IL-2 Ra Monoclonal Antibody (Catalog # MAB10202). The ND50 is typically 0.2-2.0 µg/mL.
Preparation and Storage
- 12 months from date of receipt, -20 to -70 °C as supplied.
- 1 month, 2 to 8 °C under sterile conditions after reconstitution.
- 6 months, -20 to -70 °C under sterile conditions after reconstitution.
Background: CD25/IL-2R alpha
IL-2 receptor alpha (IL-2R 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). Human IL-2R alpha cDNA encodes a 213 amino acid (aa) precursor with a 21 aa signal peptide and a 192 aa extracellular region. The ECD of Human IL-2R alpha shares a 59% amino acid sequence identity with the ECD of mouse and rat IL-2R alpha, respectively. IL‑2R alpha is primarily expressed on activated T cells and on regulatory T cells (Treg) (1-3). IL-2R beta (CD122) and gamma c (IL-2R gamma /CD132) dimerize to form a constitutively expressed intermediate affinity IL-2 receptor (4, 5). By itself, IL-2R alpha binds IL-2 with low affinity. IL-2R alpha makes no contacts with IL-2R beta or gamma c, and only minor changes are observed in the IL-2 structure in response to receptor binding. These findings support the principal role of IL-2R alpha to deliver IL-2 to the signaling complex and act as regulator of signal transduction (6, 7). A soluble form of IL‑2R alpha can be generated by proteolytic cleavage of the cell surface receptor, rendering the T cell unresponsive to IL-2 (8, 9). Increased serum levels of soluble IL‑2R alpha are found in some cancers and immune disorders (10). IL-2R alpha is required for activation induced cell death (AICD) of naive T cells, a mechanism responsible for deleting autoreactive T cell clones (11, 12). IL-2R alpha is also required for the development of CD4+CD25+ Treg which suppresses autoreactive CD4+ T cells, thereby contributing to peripheral T cell homeostasis (11-13).
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- Almeida, A.R.M. et al. (2002) J. Immunol. 169:4850.
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