|Recombinant Mouse IL-25 protein (Catalog#50138-M07H)|
|0.2 μm filtered solution in PBS with 5% trehalose|
|Produced in rabbits immunized with purified, recombinant Mouse IL-25 / IL-17E (rM IL-25; Catalog#50138-M07H; NP_542767.1; Val17 1-Ala 169). Total IgG was purified by Protein A affinity chromatography.|
|Mouse IL-25 / IL-17E|
ELISA: 0.5-1.0 μg/mL
This antibody can be used at 0.5-1.0 μg/mL with the appropriate secondary reagents to detect Mouse IL-25. The detection limit for Mouse IL-25 is 0.00245 ng/well.
|This antibody can be stored at 2℃-8℃ for one month without detectable loss of activity. Antibody products are stable for twelve months from date of receipt when stored at -20℃ to -70℃. Preservative-Free.|
Sodium azide is recommended to avoid contamination (final concentration 0.05%-0.1%). It is toxic to cells and should be disposed of properly. Avoid repeated freeze-thaw cycles.
Interleukin-25 (IL-25) is a cytokine that shares sequence similarity with interleukin 17. This cytokine can induce NF-kappaB activation, and stimulate the production of interleukin 8. Both this cytokine and interleukin 17B are ligands for the cytokine receptor IL17BR. IL-25 is a member of the IL-17 family of cytokines. However, unlike the other members of this family, IL-25 promotes T helper (Th) 2 responses. IL-25 also regulates the development of autoimmune inflammation mediated by IL-17–producing T cells. IL-25 and IL-17, being members of the same cytokine family, play opposing roles in the pathogenesis of organ-specific autoimmunity. IL-25 promotes cell expansion and Th2 cytokine production when Th2 central memory cells are stimulated with thymic stromal lymphopoietin (TSLP)–activated dendritic cells (DCs), homeostatic cytokines, or T cell receptor for antigen triggering. Elevated expression of IL-25 and IL-25R transcripts was observed in asthmatic lung tissues and atopic dermatitis skin lesions, linking their possible roles with exacerbated allergic disorders. A plausible explanation that IL-25 produced by innate effector eosinophils and basophils may augment the allergic inflammation by enhancing the maintenance and functions of adaptive Th2 memory cells had been provided.