IL-21 (human):Fc (human) (rec.) (non-lytic)
The extracellular domain of human IL-21 (aa 32-162) is fused to the N-terminus of the Fc region of a mutant human IgG1.
Shows the biological function of the IL-21 moiety and exerts a prolonged circulating half-life caused by the modified Fc domain.
|Endotoxin Content||<0.06EU/μg protein (LAL test; Lonza).|
Reconstitute 50µg vial in 50µl sterile water.
Add 1X PBS to the desired protein concentration.
|Formulation||Lyophilized from 0.2μm-filtered solution in PBS.|
|Protein Negative Control|
|Other Product Data||
Non-lytic: Acts as a long lasting fusion protein which only binds to the receptor. Mutations to the complement (C1q) and FcgR I binding sites of the IgGs Fc fragment render the fusion proteins incapable of antibody directed cytotoxicity (ADCC) and complement directed cytotoxicity (CDC).
|Declaration||Manufactured by Chimerigen.|
|Shipping and Handling|
|Short Term Storage||+4°C|
|Long Term Storage||-20°C|
Avoid freeze/thaw cycles.
Centrifuge lyophilized vial before opening and reconstitution.
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-21 (IL-21) is a key factor in the transition between innate and adaptive immune responses secreted by activated T cells. The IL-21 receptor (IL-21R) is expressed in lymphoid tissue, in particular by NK, B, T and dendritic cells, macrophages and endothelial cells. Recent evidence suggests that IL-21 plays a supportive role in the proliferation of T and B cells and influences the cytolytic activity of natural killer cells. IL-21 has been shown to up-regulate genes associated with innate immunity and to inhibit the differentiation of naïve T helper cells. IL-21 specifically inhibits IFN-γ production from developing TH1 cells and is preferentially expressed by TH2 cells. Furthermore IL-21 has been identified as a growth and survival factor for human myeloma cells. IL-21/IL-21R interactions have a unique role in sequentially activating both innate and adaptive immune responses against poorly immunogenic tumors, leading to tumor rejection that is perforin dependent but IFN-γ independent.