Invitrogen™ CD217 (IL-17Ra) Monoclonal Antibody (424LTS), Functional Grade, eBioscience™, Invitrogen™

Description

Description: The 424LTS monoclonal antibody reacts with and blocks IL-17A binding to human interleukin 17 receptor A (IL-17RA, IL-17R). IL-17RA is a type I membrane protein of approximately 96 kDa (866 amino acids) and is involved in inflammatory responses to IL-17A, IL-17F and IL-17AF heterodimer. It forms heterodimeric complexes with several other members of its receptor family, including IL-17RC for IL-17A and IL-17F signaling and IL-17RC for IL-17E (IL-25) signaling. IL-17RA is ubiquitously expressed, but in leukocytes its expression is elevated on granulocytes and monocytes. Applications Reported: This 424LTS antibody has been reported for use in blocking IL-17 receptor A ligand binding. Applications Tested: The ND50 of 424LTS as measured by the inhibition of IL-6 induction in NHDF cells is 1-5 μg/mL in the presence of 3 ng/mL of recombinant Human IL-17A. Neutralization dose will vary depending on assay method, cytokine concentration, and cell type. This antibody should be carefully titrated for optimal performance in the assay of interest. Storage and handling: Use in a sterile environment. Filtration: 0.2 μm post-manufacturing filtered. Purity: Greater than 90%, as determined by SDS-PAGE. Endotoxin Level: Less than 0.001 ng/μg antibody, as determined by LAL assay. Aggregation: Less than 10%, as determined by HPLC.

Interleukin 17A (IL-17A) is a proinflammatory cytokine secreted by activated T-lymphocytes. It is a potent inducer of the maturation of CD34-positive hematopoietic precursors into neutrophils. IL-17RA is a ubiquitous type I membrane glycoprotein that binds with low affinity to IL-17A and IL-17F. IL-17A and its receptor play a pathogenic role in many inflammatory and autoimmune diseases such as rheumatoid arthritis. Defects in IL-17RA are the cause of familial candidiasis type 5 (CANDF5) which is a rare disorder with altered immune responses and impaired clearance of fungal infections.