IL-21 is a memember of the type-I cytokine family and is an immunomodulatory cytokine produced mainly by NKT, TH17 and TFH cells. Structurally, IL-21 shows homology to IL-2, IL-4, and IL-15 proteins. In TFH cells, IL-21 expression leads to autocrine signaling through the IL-21 receptor (IL-21R) and JAK/STAT3, which leads to additional transcriptional activation by Bcl6. As with IFNγ for TH1 and IL-4 for TH2 cells, IL-21 is critical for TFH cell development and effector function. This cytokine plays a role in T cell-dependent B cell differentiation into plasma cells and memory cells and 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 RORγt 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 RORγt, IL-21 also mediates the down-regulation 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.
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FC = Flow Cytometry, Intracellular Staining/Flow Cytometry; ELISA = ELISA, ELISPOT, Multiplexing Immunoassays; ICC = Immunocytochemistry; IHC = Immunohistochemistry, Immunofluorescence, Microscopy, Imaging, In Vivo Imaging; FA = Functional Assays, Bioassays, Neutralization, Depletion Studies, Biomolecule Conjugation; WB = Immunoprecipitation, Western Blotting
RUO = Research Use Only; GPR = General Purpose Reagent; ASR = Analyte Specific Reagent. Analytical and performance characteristics are not established; CE = CE-marked reagents