Human CD25/IL-2R alpha Antibody Summary
Glu22-Cys213
Accession # P01589
*Small pack size (-SP) is supplied either lyophilized or as a 0.2 µm filtered solution in PBS.
Applications
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.
Scientific Data
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.
Reconstitution Calculator
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).
- Minami, Y. et al. (1993) Annu. Rev. Immunol. 11:245.
- Kovanen, P.E. and Leonard, W.J. (2004) Immunol. Rev. 202:67.
- Bluestone, J.A. and Tang, Q. (2005) Curr. Opin. Immunol. 17:638.
- Hatakeyama, M. et al. (1989) Science 244:551.
- Takeshita, T. et al. (1992) Science 257:379.
- Stauber, D. et al. (2006) Proc. Natl. Acad. Sci. U. S. A. 103:2788.
- Wang, X. et al. (2005) Science 310:1159.
- Wagner, D.K. et al. (1986) J. Immunol. 137:592.
- Schulz, O. et al. (1998) J. Exp. Med. 187:271.
- Witkowska, A.M. (2005) Mediat. Inflamm. 2005:121.
- Willerford, D.M. et al. (1995) Immunity 3:521.
- Van Parijs, L. et al. (1997) J. Immunol. 158:3738.
- Almeida, A.R.M. et al. (2002) J. Immunol. 169:4850.
Product Datasheets
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