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CD127 / IL-7RA Antibody, Rabbit PAb, Antigen Affinity Purified

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Mouse IL7RA/CD127 Antibody Product Information
Immunogen:Recombinant Mouse CD127 / IL-7RA protein (Catalog#50090-M08H)
Clone ID:
Ig Type:Rabbit IgG
Concentration:
Formulation:0.2 μm filtered solution in PBS with 5% trehalose
Preparation:Produced in rabbits immunized with purified, recombinant Mouse CD127 / IL-7RA (rM CD127 / IL-7RA; Catalog#50090-M08H; NP_032398.3; Met 1-Asp 239). CD127 / IL-7RA specific IgG was purified by Mouse CD127 / IL-7RA affinity chromatography.
Mouse IL7RA/CD127 Antibody Usage Guide
Specificity:Mouse CD127 / IL-7RA
Application:ELISA

ELISA: 0.1-0.2 μg/mL

This antibody can be used at 0.1-0.2 μg/mL with the appropriate secondary reagents to detect Mouse IL7R. The detection limit for Mouse IL7R is approximately 0.00245 ng/well.

Storage:This antibody can be stored at 2℃-8℃ for one month without detectable loss of activity. Antibody products are stable for twelve months from date of receipt when stored at -20℃ to -70℃. Preservative-Free.
Sodium azide is recommended to avoid contamination (final concentration 0.05%-0.1%). It is toxic to cells and should be disposed of properly. Avoid repeated freeze-thaw cycles.
Other IL7RA/CD127 Antibody Products
IL7R/IL-7R/CD127 Background

Interleukin 7 Receptor alpha (IL-7RA), also known as CD127, is a 75 kDa hematopoietin receptor superfamily member that plays an important role in lymphocyte differentiation, proliferation, and survival. IL-7 receptor alpha (CD127) signaling is essential for T-cell development and regulation of naive and memory T-cell homeostasis. IL-7RA is critically required for the proper development and function of lymphoid cells. Therefore, the IL-7RA is critically required for the proper development and function of lymphoid cells. Studies from both pathogenic and controlled HIV infection indicate that the containment of immune activation and preservation of CD127 expression are critical to the stability of CD4(+) T cells in infection. A better understanding of the factors regulating CD127 expression in HIV disease, particularly on T(CM) cells, might unveil new approaches exploiting the IL-7/IL-7R receptor pathway to restore T cell homeostasis and promote immune reconstitution in HIV infection. Factors relevant to HIV infection that could potentially decrease CD127 expression on human CD8(+) T cells. CD127 down-regulation may be an important contributor to HIV-associated T-cell dysfunction. In addition to IL-7, IL-7RA also associates with TSLPR to form the functional receptor for thymic stromal lymphopoietin (TSLP) which indirectly regulates T cell development by modulating dendritic cell activation. Mutations in the human IL-7RA gene cause a type of severe combined immunodeficiency in which the major deficiencies are in T cell development, whereas B and NK cells are relatively normal in number. Variation in the IL7RA gene was recently found associated with multiple sclerosis (MS). The polymorphisms in the IL7RA gene is involved in MS pathogenesis and suggest that IL7RA variation may primarily affect chronic disease courses. Soluble CD127 (sCD127) appears to play an important role in the immunopathogenesis of several chronic infections, multiple sclerosis, and various cancers.

Mouse IL7R/IL-7R/CD127 References
  • Vranjkovic A, et al. (2007) IL-7 decreases IL-7 receptor alpha (CD127) expression and induces the shedding of CD127 by human CD8+ T cells. Int Immunol. 19(12): 1329-39.
  • Kiazyk SA, et al. (2008) Loss of CD127 expression links immune activation and CD4(+) T cell loss in HIV infection. Trends Microbiol. 16(12): 567-73.
  • Akkad DA, et al. (2009) Variation in the IL7RA and IL2RA genes in German multiple sclerosis patients. J Autoimmun. 32(2): 110-5.
  • Crawley AM, et al. (2010) Soluble IL-7R alpha (sCD127) inhibits IL-7 activity and is increased in HIV infection. J Immunol. 184(9): 4679-87.
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