IL-23 (mouse):Fc (human) (rec.)
The mouse IL-23 complex composed of the p40 subunit (aa 23-335) and the p19 subunit (aa 20-196) is fused through a polypeptide linker to the Fc region of human IgG1.
|Endotoxin Content||<0.06EU/μg protein (LAL test; Lonza).|
|Reconstitution||Reconstitute at 100μg/ml in sterile PBS.|
|Formulation||Lyophilized from 0.2μm-filtered solution in PBS.|
|Protein Negative Control|
|Other Product Data|
|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-23 (IL-23) is a heterodimeric cytokine composed of two disulfide-linked subunits, a p19 subunit that is unique to IL-23, and a p40 subunit that is shared with IL-12 (1-5). Although p19 is expressed by activated macrophages, dendritic cells, T cells, and endothelial cells, only activated macrophages and dendritic cells express p40 concurrently to produce IL-23. The functional IL-23 receptor complex consists of two receptor subunits, the IL-12 receptor β 1 subunit (IL-12 Rβ1) and the IL-23-specific receptor subunit (IL-23 R). IL-23 has biological activities that are similar to, but distinct from IL-12. Both IL-12 and IL-23 induce proliferation and IFN-γ production by human T cells. While IL-12 acts on both naie and memory human T cells, the effects of IL-23 is restricted to memory T cells. In mouse, IL-23 but not IL-12, has also been shown to induce memory T cells to secret IL-17, a potent proinflammatory cytokine. IL-12 and IL-23 can induce IL-12 production from mouse splenic DC of both the CD8-and CD8+ subtypes, however only IL-23 can act directly on CD8+ DC to mediate immunogenic presentation of poorly immunogenic tumor/self peptide.
- Myeloid Cell–Intrinsic IRF5 Promotes T Cell Responses through Multiple Distinct Checkpoints In Vivo, and IRF5 Immune-Mediated Disease Risk Variants Modulate These Myeloid Cell Functions: J. Yan, et al.; J. Immunol. ahead of print (2020)