To order chemicals, medical devices, or other restricted products, please provide identification that includes your business name and shipping address via email [email protected] or fax 484.881.5997 referencing your VWR account number. Acceptable forms of identification are:
- • Issued document with your organization's Federal Tax ID Number
- • Government issued document with your organization's Resale Tax ID Number
- • Any other Government ID that includes the business name and address
Avantor will not lift restrictions for residential shipping addresses.
Specifications
- Protein/peptide type:Recombinant
- Species:Mouse
- Size:25 µg
- Protein/peptide name:IL-17A
- Purity:≥95%
- Cat. no.:MSPP-780331006
Specifications
About this item
Interleukin 17A (IL-17A) is the founding member of the family of cytokines that includes Interleukin 17B through Interleukin 17F. It is a potent proinflammatory cytokine that plays a key role in defense against pathogens. IL-17A and IL-17F signal as homodimers or heterodimers through the same receptor, and activate NF-kB, MAPK, and C/EBP pathways (Gaffen). IL-17A receptor is expressed on a variety of cell types, including hematopoietic cell compartments. IL-17A is produced by T helper 17 cells, CD8+ T cells, γδ T cells, natural killer T cells, B cells, neutrophils, innate lymphoid cells and mesenchymal stromal cells (MSCs; Zenobia and amp; Hajishengallis; Mojsilovic et al.). IL-17A receptor is expressed at particularly high levels on stromal cells, including MSCs. IL-17A increases the frequency and the average size of colony-forming units-fibroblast derived from bone marrow, as well as the proliferation of bone marrow-derived MSCs. IL-17A suppresses osteogenic differentiation and bone formation of bone marrow-derived MSCs. The action of IL-17A on hematopoiesis is deeply reliant on the microenvironment and the induction of other regulators. In healthy mouse bone marrow, IL-17A stimulates myeloid and early stage erythroid progenitor cells but inhibits late stage erythroid progenitor cells (Mojsilovic et al.).