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.