Invitrogen™ Human IL-21 ELISA Kit

Description

The Human Interleukin-8 (Neutrophil Activating Peptide-1) (Hu IL-8) ELISA quantitates Hu IL-8 in human serum, plasma, amniotic fluid, or cell culture medium. The assay will exclusively recognize both natural and recombinant Hu IL-8. Principle of the method The Human IL-8 solid-phase sandwich ELISA (enzyme-linked immunosorbent assay) is designed to measure the amount of the target bound between a matched antibody pair. A target-specific antibody has been pre-coated in the wells of the supplied microplate. Samples, standards, or controls are then added into these wells and bind to the immobilized (capture) antibody. The sandwich is formed by the addition of the second (detector) antibody, a substrate solution is added that reacts with the enzyme-antibody-target complex to produce measurable signal. The intensity of this signal is directly proportional to the concentration of target present in the original specimen. Rigorous validation Each manufactured lot of this ELISA kit is quality tested for criteria such as sensitivity, specificity, precision, and lot-to-lot consistency. See manual for more information on validation.

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.