IL-35 (mouse):Fc (human) (rec.)
A soluble dimeric fusion protein consisting of the extracellular domain of mouse IL12a subunit (aa 23-215) is fused to the Fc region of human IgG1, and the mouse Ebi3 subunit (aa 23-228) linked to IL12a by disulfide bonds.
Bioactivity was measured in a cell proliferation assay of Con A activated mouse splenocytes.
|Endotoxin Content||<1EU/mg 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|
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-35 (IL-35) is a novel IL-12 family cytokine produced by regulatory T cells (Treg) but not by resting or activated effector T cells (Teff). IL-35 is a heterodimeric protein composed of EBI3 (Epstein-Barr-Virus-induced gene 3) and IL-12a (p35). EBI3 is a downstream target of Foxp3, a transcription factor required for Treg-cell development and function, and thus Treg-cell restriction of IL35 occurs. Regulatory T cells are essential for maintaining self tolerance and preventing autoimmunity, and IL-35 is identified as a molecule that mediates the immune suppression function of Treg-cell. As an inhibitory cytokine, IL-35 induces proliferation of Treg-cell populations but suppresses Th17 cell development. Studies in mice show the absence of either IL-35 chain from Treg-cell reduces the cells' ability to suppress inflammation using an experimental model for inflammatory bowel disease. IL-35 is suggested as a potential target of immunotherapy. Recently, insufficient IL-35 levels were shown to play a pivotal role in the development of type 1 diabetes (T1D) and autoimmune diseases.
- Interleukin-35 administration counteracts established murine type 1 diabetes - possible involvement of regulatory T cells: K. Singh, et al.; Sci. Rep. 5, ID12633 (2015)
- Cytokine modulation by IL-35 in mice with allergic rhinitis: M. Yokota, et al.; Am. J. Rhinol. Allergy 29, 251 (2015)
- Remission of systemic lupus erythematosus disease activity with regulatory cytokine interleukin (IL)-35 in Murphy Roths Large (MRL)/lpr mice: Z. Cai, et al.; Clin. Exp. Immunol. 181, 253 (2015)
- Intranasal administration of IL-35 inhibits allergic responses and symptoms in mice with allergic rhinitis: M. Suzuki, et al.; Allergol. Int. 66, 351 (2017)
- IL-35 suppresses lipopolysaccharide-induced airway eosinophilia in EBI3-deficient mice: K. Kanai, et al.; J. Immunol. 198, 119 (2017)
- The unknown aspect of BAFF: Inducing IL-35 production by a CD5+CD1dhiFcγRIIbhi regulatory B-Cell subset in lupus: Y. Zhang, et al.; J. Invest. Dermatol. 137, 2532 (2017)
- IL-35 induces N2 phenotype of neutrophils to promote tumor growth: J.-M. Zou, et al.; Oncotarget 8, 33501 (2017)
- Regulatory T cells and their derived cytokine, interleukin-35, reduce pain in experimental autoimmune encephalomyelitis: S.S. Duffy, et al.; J. Neurosci. 39, 2326 (2019)
- Elevated interleukin-35 suppresses liver inflammation by regulation of T helper 17 cells in acute hepatitis B virus infection: D.K. Teng, et al.; Int. Immunopharm. 70, 252 (2019)
- Interleukin-33 activates regulatory T cells to suppress innate γδ T cell responses in the lung: L.D. Fasutino, et al. Nat. Immunol. 21, 1371 (2020)
- Elevation in the counts of IL-35-producing B cells infiltrating into lung tissue in mycobacterial infection is associated with the downregulation of Th1/Th17 and upregulation of Foxp3 + Treg: C. Chen, et al.; Sci. Rep. 10, 13212 (2020)
- B cell–Derived IL35 Drives STAT3-Dependent CD8+ T-cell Exclusion in Pancreatic Cancer: B. Mirlekar, et al.; Cancer Immunol. Res. 8, 292 (2020)
- Interleukin 35 delays hindlimb ischemia-induced angiogenesis through regulating ROS-extracellular matrix but spares later regenerative angiogenesis: H. Fu, et al.; Front. Immunol. 11, 595813 (2020)