IL-4 (mouse):Fc (mouse) (rec.) (non-lytic)
|Synonyms||Interleukin-4; B Cell Stimulatory Factor 1; BSF-1|
The extracellular domain of mouse IL-4 (aa 21-140) is fused to the N-terminus of the Fc region of a mutant mouse IgG2a.
Shows the biological function of the IL-4 moiety and exerts a prolonged circulating half-life caused by the modified Fc domain.
|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||
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-4 (IL-4) is a cytokine produced by type 2 helper T cells, the Th2 cells. These cells tends to make a specific set of lymphokines including IL-4, IL-5, IL-6, IL-10, IL-13, IL-3 and GM-CSF and fail to produce IL-2, IFN-γ, and lymphotoxin (TNF-β). In addition, mast cells can produce IL-4. IL-4 exerts numerous effects on various hematopoietic cell types. On B cells, IL-4 promotes immunoglobulin class switching to IgE and IgG1 isotypes and upregulates MHC class II and CD23 expression. IL-4 promotes survival, growth, and differentiation of both T and B lymphocytes, mast cells and endothelial cells. In addition, IL-4 inhibits the production of TNF, IL-1, and IL-6 by macrophages.
- Administration of noncytolytic IL-10/Fc in murine models of lipopolysaccharide-induced septic shock and allogeneic islet transplantation: X.X. Zheng, et al.; J. Immunol. 154, 5590 (1995)
- Prolonged islet allograft acceptance in the absence of interleukin 4 expression: P. Nickerson, et al.; Transpl. Immunol. 4, 81 (1996)
- Physiological mechanisms of regulating alloimmunity: cytokines, CTLA-4, CD25+ cells, and the alloreactive T cell clone size: M. Sho, et al.; J. Immunol. 169, 3744 (2002)