Measured in a cell proliferation assay using MC/9 mouse mast cells. The ED50 for this effect is typically 0.15-0.9 ng/mL.

IL-9 Protein, Mouse, Recombinant (His) is expressed in Baculovirus insect cells with His tag. The predicted molecular weight is 15.6 kDa and the accession number is P15247.

Mouse

Baculovirus Insect Cells

Il-9,interleukin 9,P40

The Mouse IL9 (NP_032399.1) (Met1-Pro144) was expressed with a polyhistidine tag at the C-terminus.

> 95 % as determined by SDS-PAGE.

A Certificate of Analysis (CoA) containing reconstitution instructions is included with the products. Please refer to the CoA for detailed information.

It is recommended to store recombinant proteins at -20°C to -80°C for future use. Lyophilized powders can be stably stored for over 12 months, while liquid products can be stored for 6-12 months at -80°C. For reconstituted protein solutions, the solution can be stored at -20°C to -80°C for at least 3 months. Please avoid multiple freeze-thaw cycles and store products in aliquots.

Interleukin 9, also known as IL-9, is a cytokine (cell signaling molecule) belonging to the group of interleukins. IL-9 is a cytokine that acts as a regulator of a variety of hematopoietic cells. This cytokine stimulates cell proliferation and prevents apoptosis. It functions through the interleukin 9 receptor (IL-9R), which activates different signal transducer and activator (STAT) proteins and thus connects this cytokine to various biological processes. Genetic studies on a mouse model of asthma demonstrated that this cytokine is a determining factor in the pathogenesis of bronchial hyperresponsiveness. IL-9 is a key molecule that affects the differentiation of TH17 cells and Treg function. IL-9 predominantly produced by TH17 cells synergizes with TGF-β1 to differentiate naive CD4+ T cells into TH17 cells, while IL-9 secretion by TH17 cells is regulated by IL-23. Interestingly, IL-9 enhances the suppressive functions of FoxP3+ CD4+ Treg cells in vitro, and the absence of IL-9 signaling weakens the suppressive activity of nTregs in vivo, leading to an increase in effector cells and worsening of experimental autoimmune encephalomyelitis. The mechanism of IL-9 effects on TH17 and Tregs is through activation of STAT3 and STAT5 signaling. Our findings highlight the role of IL-9 as a regulator of pathogenic versus protective mechanisms of immune responses.