CD25/IL-2R alpha Antibody [Alexa Fluor™ Plus 680]

• Clonality: Polyclonal
• Host: Goat
• Conjugate: Alexa Fluor Plus 680

CD25/IL-2R alpha Antibody [Alexa Fluor™ Plus 680] Summary

• Specificity: Detects mouse CD25/IL-2 R alpha in ELISAs and Western blots.
• Isotype: IgG
• Clonality: Polyclonal
• Host: Goat

Packaging, Storage & Formulations

• Storage: Protect from light. Do not freeze. 12 months from date of receipt, 2 to 8 °C as supplied
• Buffer: Supplied 0.2 mg/mL in a saline solution containing BSA and Sodium Azide.

Notes

This product is produced by and ships from R&D Systems, Inc., a Bio-Techne brand.

Background

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) (1-3). 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 (4, 5). 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 (6, 7). 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 (8). 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 (9, 10). Increased serum levels of soluble IL-2 R alpha are found in some cancers and immune disorders (11). 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 (12, 13). 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 (12-14).

1. Minami, Y. et al. (1993) Annu. Rev. Immunol. 11:245.
2. Kovanen, P.E. and W.J. Leonard (2004) Immunol. Rev. 202:67.
3. Bluestone, J.A. and Q. Tang (2005) Curr. Opin. Immunol. 17:638.
4. Miller, J. et al. (1985) J. Immunol. 134:4212.
5. Shimuzu, A. et al. (1985) Nucleic Acids Res. 13:1505.
6. Hatakeyama, M. et al. (1989) Science 244:551.
7. Takeshita, T. et al. (1992) Science 257:379.
8. Wang, X. et al. (2005) Science 310:1159.
9. Wagner, D.K. et al. (1986) J. Immunol. 137:592.
10. Schulz, O. et al. (1998) J. Exp. Med. 187:271.
11. Witkowska, A.M. (2005) Mediat. Inflamm. 2005:121.
12. Willerford, D.M. et al. (1995) Immunity 3:521.
13. Van Parijs, L. et al. (1997) J. Immunol. 158:3738.
14. Almeida, A.R.M. et al. (2002) J. Immunol. 169:4850.

Limitations

This product is for research use only and is not approved for use in humans or in clinical diagnosis. Primary Antibodies are guaranteed for 1 year from date of receipt.