IL-35 (human):Fc (human) (rec.)
The human IL-35 complex composed of the Ebi3 subunit (aa 21-229) and the IL-12a (p35) subunit (aa 57-253) is fused through a polypeptide linker to the Fc portion of human IgG1.
Bioactivity was measured in a cell proliferation assay using anti-CD3 activated human peripheral mononuclear cells.
|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-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.
- EBI3 downregulation contributes to type I collagen overexpression in scleroderma skin: H. Kudo, et al.; J. Immunol. 195, 3565 (2015)
- A potential immunopathogenic role for reduced IL-35 expression in allergic asthma: W. Wang, et al.; J. Asthma 52, 763 (2015)