Human IL-18/IL-18 BPa Complex DuoSet ELISA

Key Product Details

Product Specifications

Kit Contents for Human IL-18/IL-18 BPa Complex DuoSet ELISA

Other Reagents Required

DuoSet Ancillary Reagent Kit 2 (5 plates): (Catalog # DY008) containing 96 well microplates, plate sealers, substrate solution, stop solution, plate coating buffer (PBS), wash buffer, and Reagent Diluent Concentrate 2.

The components listed above may be purchased separately:
PBS: (Catalog # DY006), or 137 mM NaCl, 2.7 mM KCl, 8.1 mM Na₂HPO₄, 1.5 mM KH₂PO₄, pH 7.2 - 7.4, 0.2 µm filtered

Wash Buffer: (Catalog # WA126), or 0.05% Tween^® 20 in PBS, pH 7.2-7.4
Reagent Diluent: (Catalog # DY995), or 1% BSA in PBS, pH 7.2-7.4, 0.2 µm filtered

Substrate Solution: 1:1 mixture of Color Reagent A (H₂O₂) and Color Reagent B (Tetramethylbenzidine) (Catalog # DY999)

Stop Solution: 2 N H₂SO₄ (Catalog # DY994)

Microplates: R&D Systems (Catalog # DY990)

Plate Sealers: ELISA Plate Sealers (Catalog # DY992)

Preparation and Storage

Background: IL-18/IL-18 BPa Complex

Interleukin 18 (IL-18), also known as interferon-gamma-inducing factor (IGIF) and IL-1γ, is a cytokine which shares biologic activities with IL-12 and structural similarities with the IL-1 family of proteins. IL-18 was originally cloned from liver cells and has since been shown to be expressed by monocyte/macrophages, osteoblasts and keratinocytes. Caspase-1 (IL-1 beta-converting enzyme) has been implicated in the physiological processing of pro-IL-18 to IL-18. Similarly to IL-12, human IL-18 has been shown to enhance NK cell activity in PBMC cultures. Human IL-18 has also been found to induce the production IFN-γ and GM-CSF while inhibiting the production of IL-10 by PBMC. On enriched human T cells, human IL-18 can enhance Th1 cytokine production and stimulate cell proliferation via an IL-2-dependent pathway. In the mouse system, IL-18 has been shown to be a costimulatory factor for the activation of Th1, but not Th2, cells. IL-18 was found to selectively enhance the FasL-mediated cytotoxicity of Th1, but not Th0 or Th2, cells. IL-18 has also been shown to induce activated B cells to produce IFN-γ that inhibits IgE production.

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