Invitrogen™ IL-21 Monoclonal Antibody (eBio3A3-N2 (3A3-N2)), eBioscience™, Invitrogen™

Description

Description: The monoclonal antibody eBio3A3-N2 reacts with human IL-21, a potent stimulator of NK and cytolytic T cells. IL-21 is a 131 amino acid protein most closely related to IL-2 and IL-15. Expression is found in CD4+ cells upon activation. In addition to its effect on NK cells, IL-21 stimulates proliferation of B-cell stimulated by crosslinking of the CD40 antigen and stimulates the proliferation of bone marrow progenitor cells and the expression of the NK-cell marker CD56 in the presence of IL-15. Applications Reported: The eBio3A3-N2 antibody has been reported for use in ELISA capture of IL-21 analysis. Applications Tested: The eBio3A3-N2 antibody has been tested as the capture antibody in a sandwich ELISA for analysis of human Interleukin-21 (IL-21) in combination with the biotin eBio2B2-G20 (cat.13-7218) antibody for detection and recombinant standard human IL-21 (cat. 39-8219) as the standard. A suitable range of concentrations of this antibody for ELISA capture is 1-4 μg/mL. A standard curve consisting of doubling dilutions of the recombinant standard over the range of 4000 pg/mL - 60 pg/mL should be included in each ELISA plate. Purity: Greater than 90%, as determined by SDS-PAGE. Aggregation: Less than 10%, as determined by HPLC. Filtration: 0.2 μm post-manufacturing filtered.

IL-21 is a 17 kDa immunomodulatory cytokine produced mainly by Natural Killer Cells (NKT), T helper (Th) 17 and T follicular helper (TFH) cells. In TFH cells, IL-21 expression leads to autocrine signaling through the IL-21 receptor (IL-21R) and STAT3, which leads to additional transcriptional activation by Bcl6. As with IFN gamma for Th1 and IL-4 for Th2 cells, IL-21 is critical for TFH cell development and effector function. IL-21 plays a role in T cell-dependent B cell differentiation into plasma cells and memory cells, stimulation of IgG production and induction of apoptotic signaling in naive B cells. In Th17 cells, IL-21 expression and autocrine feedback through STAT3, IRF4 and ROR gamma t lead to upregulation of the IL-23R, thereby preparing Th17 cells for maturation and maintenance by the inflammatory cytokine IL-23. While upregulating IRF4 and ROR gamma t, IL-21 also mediates the downregulation of Foxp3. IL-21 deficient mice are protected from developing colitis upon chemical treatment by their inability to upregulate Th17-associated molecules. In comparison, elevated levels of IL-21 are present in chemically-induced colitis mouse models.