Recombinant Human TNF-alpha

TNF-alpha can downregulate the macropinocytosis and the expression of surface Fc receptors of immature DCs . It also upregulates the expression of MHC class I/II molecules and B7 family molecules (such as CD80 and CD86) on the cell surface, so that immature DCs differentiate to mature DCs. At this point, the antigen uptake and processing abilities of DCs decrease significantly while the antigen presentation ability of DCs increases significantly so that DCs can activate T cells in a very effective way. TNF stimulates IL-1 secretion of monocytes and macrophages, enhances the proliferation of IL-2-dependent thymic cells and T cells, promotes the production of lymphokines such as IL-2, CSF, and IFN-gamma, and enhances the proliferation and Ig secretion of B cells stimulated by mitogens or foreign antigens. TNF-alpha can kill certain tumor cells in vivo and in vitro, or inhibit proliferation. Treatment of tumor cells (such as mouse fibroblast line L929) with actinomycin D, mitomycin C, or cycloheximide can significantly increase the activity of TNF-alpha in killing tumor cells. This improves the phagocytic ability of neutrophils, increases the production of peroxide anions, enhances ADCC effect, and stimulates cell degranulation and secretion of myeloperoxidase. Recombinant Human TNF-alpha is expressed by E. coli, and is produced with raw materials of pharmaceutical applicable level. The host protein residue, nucleic acid residue and common pathogens are strictly controlled, and the production and quality management procedures of the product comply with GMP regulations to ensure the traceability of the production process and all raw materials.