Invitrogen™ IL-21 Monoclonal Antibody (FFA21), PE, eBioscience™, Invitrogen™

Description

Description: This FFA21 monoclonal antibody reacts with mouse interleukin-21 (IL-21). IL-21 is a 17 kDa immunomodulatory cytokine produced mainly by 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, IL-4 for Th2 and IL-17A for Th17, IL-21 is critical for TFH cell effector function. This cytokine 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 maintece by the inflammatory cytokine IL-23. While upregulating IRF4 and ROR gamma t, IL-21 also mediates the downregulation of Foxp3. High levels of IL-21 are present in chemically-induced colitis models. IL-21-deficient mice are protected from developing colitis upon chemical treatment by their inability to upregulate Th17-associated molecules. Preliminary data suggest that clone FFA21 recognizes a different epitope than anti-mouse IL-21 clone mhalx21 (cat. 51-7213). Applications Reported: This FFA21 antibody has been reported for use in intracellular staining followed by flow cytometric analysis.

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.