|CTLA‑4 Inhibition of B7‑1/CD80-induced IL‑2 Secretion and Neutralization by Mouse CTLA‑4 Antibody. Recombinant Mouse CTLA‑4 Fc Chimera (Catalog # 434-CT) inhibits Recombinant Human B7‑1/CD80 Fc Chimera (Catalog # 140-B1) induced IL‑2 secretion in the Jurkat human acute T cell leukemia cell line in a dose-dependent manner (orange line), as measured by the Human IL‑2 Quantikine ELISA Kit (Catalog # D2050). Inhibition of Recombinant Human B7‑1/CD80 Fc Chimera (3 µg/mL) activity elicited by Recombinant Mouse CTLA‑4 Fc Chimera (1 µg/mL) is neutralized (green line) by increasing concentrations of Mouse CTLA‑4 Monoclonal Antibody (Catalog # MAB434). The ND50 is typically 2.5-10 µg/mL in the presence of PHA (10 µg/mL).|
CTLA-4 and CD28, together with their ligands B7-1 and B7-2, constitute one of the dominant costimulatory pathways that regulate T and B cell responses. CTLA-4 and CD28 are structurally homologous molecules that are members of the immunoglobulin (Ig) gene superfamily. Both CTLA-4 and CD28 are composed of a single Ig V‑like extracellular domain, a transmembrane domain and an intracellular domain. CTLA-4 and CD28 are both expressed on the cell surface as disulfide-linked homodimers or as monomers. The genes encoding these two molecules are closely linked on human chromosome 2. CTLA-4 was originally identified as a gene that was specifically expressed by cytotoxic T lymphocytes. However, CTLA-4 transcripts have since been found in both Th1 and Th2, and CD4+ and CD8+ T cell clones. Whereas, CD28 expression is constitutive on the surfaces of 95% of CD4+ T cells and 50% of CD8+ T cells and is down regulated upon T cell activation, CTLA-4 expression is upregulated rapidly following T cell activation and peaks approximately 24 hours following activation. Although both CTLA-4 and CD28 can bind to the same ligands, CTLA-4 binds to B7-1 and B7-2 with 20-100-fold higher affinity than CD28. The physiological role of CTLA-4 in T cell costimulation is currently being studied. Recombinant human or mouse CTLA-4/Fc chimera preparations produced at R&D Systems have been shown to bind both B7-1 and B7-2 with high affinity and to inhibit CD28 signalling competitively.
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