Ultra-LEAF™ Purified anti-human IL-18 Antibody, IL-18, W17071A,BioLegend,949703

Host

Rat

Reactivity

Human

Application

Neut - Quality tested

Platform ID

BAB017447237

BioLegend

Headquarters

8999 BioLegend Way San Diego, CA 92121 United States

Contact

Tel: 1-858-455-9588
Fax: +49 (4131) 7023913

Email:

Product Specifications
Scientific Background

Specifications

NameUltra-LEAF™ Purified anti-human IL-18 Antibody, IL-18, W17071A
Cat. No.949703
HostRat
RRIDAB_2910518 (BioLegend Cat. No. 949703)AB_2910518 (BioLegend Cat. No. 949704)
IsotypeRat IgG2a, κ
ReactivityHuman
ApplicationNeut - Quality tested
ClonalityMonoclonal
Clone NumberW17071A
ConcentrationThe antibody is bottled at the concentration indicated on the vial, typically between 2 mg/mL and 3 mg/mL. To obtain lot-specific concentration and expiration, please enter the lot number in ourCertificate of Analysisonline tool.
TargetIL-18
ImmunogenRecombinant human IL-18
PurityThe Ultra-LEAF™ (Low Endotoxin, Azide-Free) antibody was purified by affinity chromatography.
Formulation0.2 µm filtered in phosphate-buffered solution, pH 7.2, containing no preservative.
StorageThe antibody solution should be stored undiluted between 2°C and 8°C. This Ultra-LEAF™ solution contains no preservative; handle under aseptic conditions.
Regulatory StatusResearch Use Only

Scientific Background

IL-18 was first identified as IFN-β-inducing factor (IGIF). It is a member of the IL-1 family of cytokines and similar to IL-1β, IL-18 is initially synthesized as an inactive precursor without a signal peptide and is cleaved into the mature form by activated caspase 1. Caspase 1-independent maturation of IL-18 is induced by FASL. Mature IL-18 binds directly to the IL-18 receptor alpha chain and then recruits IL-18 receptor beta chain to form a high affinity complex. The high affinity complex recruits MyD88 and leads to IRAK/TRAF6 pathway activation and NF-κB nuclear translocation. IL-18 in combination with IL-12 shows a synergistic effect on IFNβ production. Without costimulation, IL-18 alone does not induce IFNβ production. IL-18 can induce IFNβ production from splenocytes, liver macrophage, T lymphocytes and natural killer cells. IL-18 also enhances the production of GM-CSF and IL-12. IL-18 enhances Th1 cell development by synergizing with IL-12 and promotes Th2 cell differentiation in the presence of TCR activation. IL-18 plays a major role in autoimmune and inflammatory diseases. It has been implicated in many diseases such as eczema, psoriasis, inflammatory bowel disease, metabolic syndromes, hemophagocytic syndrome, sepsis and acute kidney injury. Blocking of IL-18 activity has been an attractive therapeutic approach for autoimmune disease. It has been shown that neutralization of IL-18 has reduced both intestinal IFNβ and TNFα production and resulted in a dose dependent reduction in colitis severity in mice. IL-18 is also able to induce angiogenesis, migration, proliferation and immune escape, and has been associated with cancer. Several publications show that IL-18 gene polymorphism may be risk factors for several cancers.

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