Rhesus IL18 Antibody

$322.00$847.00

Catalog #: ABCESPA1426
Product Features
Immunogen: Recombinant Rhesus IL18 / Interleukin-18 Protein 
Clonality:  Mouse MAb
Cloneno: 5G10E10
Isotype: Mouse IgG2a
Buffer: 0.2 μm filtered solution in PBS with 5% trehalose
Reactivity: Cynomolgus
Specificity: Rhesus IL18 / Interleukin-18No cross-reactivity with E.coli cell lysate in ELISA
Application: ELISA
Recommend dilution:  ELISA: 0.5-1 μg/mL. This antibody can be used at 0.5-1 μg/mL with the appropriate secondary reagents to detect Rhesus IL18. The detection limit for Rhesus IL18 is approximately 0.039 ng/well.
Storage: This antibody can be stored at 2℃-8℃ for one month without detectable loss of activity. Antibody products are stable for twelve months from date of receipt when stored at -20℃ to -80℃. Preservative-Free.Sodium azide is recommended to avoid contamination (final concentration 0.05%-0.1%). It is toxic to cells and should be disposed of properly. Avoid repeated freeze-thaw cycles.
Background: Interleukin-18 (IL-18, also known as interferon-gamma inducing factor) is a proinflammatory cytokine that belongs to the IL-1 superfamily and is produced by macrophages and other cells. This cytokine can induce the IFN-gamma production of T cells. The combination of IL-18 and IL12 has been shown to inhibit IL4 dependent IgE and IgG1 production, and enhance IgG2a production of B cells. IL-18 binding protein (IL18BP) can specifically interact with this cytokine, and thus negatively regulate its biological activity. IL-18 is an IL-1−like cytokine that requires cleavage with caspase-1 to become active, was found to increase IgE production in a CD4+ T cells-, IL-4− and STAT6−dependent fashion. IL-18 and T cell receptor−mediated stimulation could induce naïve CD4+ T cells to develop into IL-4−producing cells in vitro. Thus, caspase-1 and IL-18 may be critical in regulation of IgE production in vivo, providing a potential therapeutic target for allergic disorders. IL-18 production in primary synovial cultures and purified synovial fibroblasts was, in turn, upregulated by TNF-α and IL-1β, suggesting that monokine expression can feed back to promote Th1 cell development in synovial membrane. Besides, synergistic combinations of IL-18, IL-12, and IL-15 may be of importance in sustaining both Th1 responses and monokine production in RA.
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