IL-18 (human) (rec.)
|Synonyms||Interleukin-18; Interferon-γ-inducing Factor; IGIF; IL-1γ; IL1F4|
Human IL-18 (aa 37-193) is untagged.
|Endotoxin Content||<0.06EU/μg purified protein (LAL test; Lonza).|
|Reconstitution||Reconstituted in sterile H2O not less than 100μg/ml, which can then be further diluted in other aqueous solutions.|
|Formulation||Lyophilized from 0.2μm-filtered solution in 1X PBS.|
|Other Product Data||
NCBI reference NP_001553.1: IL-18 (human)
|Declaration||Manufactured by Chimerigen.|
|Shipping and Handling|
|Short Term Storage||+4°C|
|Long Term Storage||-20°C|
|Handling Advice||Avoid freeze/thaw cycles.|
Stable for at least 1 year after receipt when stored at -20°C.
Working aliquots are stable for up to 3 months when stored at -20°C.
|Product Specification Sheet|
Interleukin-18 (IL-18) is a costimulatory factor for production of interferon-γ (IFN-γ) in response to toxic shock and shares functional similarities with IL-12. IL-18 is synthesized as a precursor 24kDa molecule without a signal peptide and must be cleaved to produce an active molecule. IL-1 converting enzyme (ICE; Caspase-1) cleaves pro-IL-18 at aspartic acid in the P1 position, producing the mature, bioactive peptide that is readily released from the cells. It is reported that IL-18 is produced from Kupffer cells, activated macrophages, keratinocytes, intestinal epithelial cells, osteoblasts, adrenal cortex cells and murine diencephalon. IFN-γ is produced by activated T or NK cells and plays critical roles in the defense against microbiral pathogens. IFN-γ activates macrophages and enhances NK activity and B cell maturation, proliferation and Ig secretion. IFN-γ also induces expression of MHC class I and II antigens and inhibits osteoclast activation. IL-18 acts on T helper type-1 (Th1) T cells and in combination with IL-12 strongly induces them to produce IFN-γ. Pleiotropic effects of IL-18 have also been reported, such as enhancement production of IFN-γ and GM-CSF in peripheral blood mononuclear cells, production of Th1 cytokines, IL-2, GM-CSF, IFN-γ in T cells and enhancement of Fas ligand expression by Th1 cells.