EBI3 (IL-27 subunit) Monoclonal Antibody (ebic6), PE, eBioscience™, Invitrogen™

Description

Description: This ebic6 monoclonal antibody reacts with human Epstein-Barr Virus Induced Gene 3 (EBI3). EBI3 can be expressed and secreted as monomers or homodimers, and was first identified in virally-infected B cells. It is also believed to be secreted as a homodimer by cells of the trophoblast, where it may play a role in immune tolerance during pregcy. Additionally, EBI3 is a component of two of the four members of the interleukin (IL)-12 family of heterodimeric cytokines. EBI3 was first found to heterodimerize with p28 (IL-30) to form IL-27, which is secreted by antigen-presenting cells in response to pro-inflammatory stimuli. IL-27 has been shown to have both pro-inflammatory and anti-inflammatory effects. It influences the commitment of CD4+ T-cells toward the Th1 lineage by inducing the expression of the T-bet transcription factor and the upregulation of IL-12R beta 2. Its anti-inflammatory functions include the suppression of Th2 and Th17 proliferation and differentiation. More recently, EBI3 was also found to dimerize with the IL-12 subunit, p35 to form IL-35. The biology of IL-35 is incompletely understood, but it is believed to be unique among the IL-12 family members in its expression and function. It is produced by regulatory T cells, and appears to have immunoregulatory functions.

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.