Invitrogen™ IL-28A Human ELISA Kit

Beschreibung

The Human Interleukin 28A (Hu IL-28A) ELISA quantitates Hu IL-28A in human serum, plasma, or cell culture medium. The assay will exclusively recognize both natural and recombinant Hu IL-28A. Principle of the method The Human IL-28A 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-28A belongs to the IFN lambda family, a novel family of cytokines within the IL-10 superfamily. The three members of this family are IL-29 (IFN lambda 1), IL-28A (IFN lambda 2), and IL-28B (IFN lambda 3), and are also known as the type III Interferons.The IFN lambdas signal through a heterodimeric receptor of which one subunit, IL-10R2, is shared with other members of the superfamily. The second subunit, IFN lambda R1 or IL-28R alpha, is unique to the IFN lambdas. Signaling occurs through the Jak/STAT pathway in a similar manner as the type I IFN (IFN alpha/beta) and activates many of the same genes despite low sequence homology between the cytokines and receptors in the two families. Both IFN families display antiviral activity through the induction of antiviral protein production in target cells and the upregulation of MHC class I expression. These proteins also exhibit antiproliferative and antitumor effects, making them a possible alternative to IFN alpha cancer therapies. Unlike the type I IFN, which are able to stimulate most cells, response to IFN lambda stimulation appears to be limited to dendritic and some tumor cells due to the limited expression of IFN lambda R1. Another notable difference is the ability of the IFN lambda stimulation to drive dendritic cells towards the production of CD4+CD25+FoxP3+ regulatory T cells, suggesting a possible immunoregulatory role.