Invitrogen™ EBI3 (IL-27 subunit) Monoclonal Antibody (DNT27), eBioscience™, Invitrogen™

Description

Description: The monoclonal antibody DNT27 reacts with mouse Epstein-Barr Virus-induced gene 3 (EBI3). EBI3 is a 34 kDa soluble protein first identified in B cells that is upregulated after Epstein-Barr virus infection. EBI3 can exist as a homodimer and also heterodimerizes with IL-27alpha (p28, IL-30) to form the cytokine IL-27. IL-27 is produced most abundantly by dendritic cells and macrophages with some recent reports of expression in NKT cells. Recently, a complex of EBI3 and the p35 subunit of IL-12, called IL-35, has been reported to be produced by regulatory T cells. Applications Reported: This DNT27 antibody has been reported for use in immunoblotting (WB). Applications Tested: This DNT27 antibody has been tested by western blot of cell lysates prepared from mouse EBI3-transfected 293T cells and bone marrow-derived dendritic cells. This can be used at less than or equal to 1-5 μg/mL. It is recommended that the antibody be carefully titrated for optimal performance in the assay of interest. Purity: Greater than 90%, as determined by SDS-PAGE. Aggregation: Less than 10%, as determined by HPLC. Filtration: 0.2 μm post-manufacturing filtered.

EBI3 (Epstein-Barr virus Induced-3) is a secreted glycoprotein of the hematopoietin receptor family. It plays a critical regulatory role in the induction of Th2-type immune responses and the development of Th2-mediated tissue inflammation in vivo, which may be mediated through the control of iNKT cell function. EBI3 dimerizes with p28 and p35 subunits of IL-12 to form new proteins IL-27 and IL-35, respectively. IL-27 is an early product of activated antigen presenting cell that is produced upon TLR ligation. It negatively regulates Th17 cell differentiation. EBI3 is widely expressed and its expression in dendritic cell is transcriptionally regulated by TLR signaling via MyD88 and NF-kappaB during innate immune responses preceding cytokine driven Th cell development. EBI3 signal inhibits delayed-type hypersensitivity responses by suppressing IL-17 production and inducing IL-10 hyperproduction. EBI3 may play a novel role in controlling tumor metastasis via lung CD8+ T cells, and its deficiency is associated with a diminished production of Th2 cytokines which are known to regulate allergic airway inflammation in asthma. Targeted deletion of EBI3 protects mice from lung metastasis.