Description: The antibody eBio473P19 reacts with the p19 subunit of human IL-23. The eBio473P19 antibody was generated from immunization with authentic, insect cell-expressed, recombinant human IL-23 heterodimer.
The use of a p19-specific capture antibody and a p40-specific detection antibody yields a human IL-23 sandwich ELISA exquisitely specific for human IL-23. IL-12 p40 monomer and IL-12 p70 were run in the assay at 200 ng/ml with no interference or cross-reactivity observed. A panel of 20 unrelated cytokines was also run in the IL-23 ELISA at 100 ng/ml with no cross reactivity observed. The assay has been validated by specific detection of significant levels of native human IL-23 protein in supernatants from a variety of different activated dendritic cell populations.
IL-23 is a heterodimeric cytokine composed of the p40 subunit of IL-12 disulfide-linked with a protein p19. p19, like p35 of IL-12, is biologically inactive by itself. IL-23 interacts with IL-12Rbeta1 and an additional, novel beta2-like receptor subunit with STAT4 binding domain, termed IL-23R. IL-23 is secreted by activated mouse and human dendritic cells. Biological activities of mouse IL-23 are distinct from those of mouse IL-12. Mouse IL-23 was found not to induce significant amounts of IFN-g. Mouse IL-23 does induce strong proliferation of memory T cells (but not naïve T cells), whereas IL-12 has no effect on memory cells. Additionally, mouse IL-23 (but not IL-12) can activate mouse memory T cells to produce the proinflammatory cytokine IL-17. Human IL-23 has biological properties which are less distinct from human IL-12; human IL-23 induces proliferation of memory T cells and induces moderate levels of IFN-g production by naïve and memory T cells, as compared to IL-12. IL-23-dependent, IL-17-producing CD4+ T cells (Th-17 cells) have been identified as a unique subset of Th cells that develops along a pathway that is distinct from the Th1- and Th2- cell differentiation pathways. The hallmark effector molecules of Th1 and Th2 cells, e.g., IFN-g and IL-4, have each been found to negatively regulate the generation of these Th-17 cells. More recently, de novo differentiation of Th-17 cells in the absence of IL-23 has been demonstrated by treatment of naïve CD4 cells with TGF beta1 and IL-6.