Recombinant Human IL-10 Protein (N-His Tag)

IL-10 affects the main functions of monocyte macrophages: release of immune mediators, antigen presentation. Briefly, it inhibits the function of mononuclear macrophages to promote natural and specific immunity while enhancing these cellular inhibition, immune tolerance induction, and scavenger function. IL-10 inhibits antigen presentation by mononuclear macrophages. It can reduce the expression of IL-IFN-γ-induced MHCII molecules and costimulatory molecules (e.g. CD86) and adhesion molecules (e.g. CD54) . Furthermore, IL-10 inhibits the synthesis of IL-12 and, therefore, blocks the Th1 immune response. The direct inhibitory effect on APC is enhanced by inhibition by CD4+T. For example, IL-10 causes APC to inhibit IL-12 synthesis, resulting in a decrease in the number of T cells producing IFN-γ. In addition, IL-10 itself inhibits the production of IFN-γ in Th1 cells, and IFN-γ deficiency enhances the inactivation of APC. IL-10 also reduces macrophage secretion of IL-23, a cytokine essential for Th17 cell immunity. IL-10 also inhibits the killing of microorganisms that are ingested. This increase in phagocytosis of the pathogen theoretically increases the likelihood that the cell will be attacked by complement, but it appears that IL-10 reduces this risk: it protects human monocyte macrophages from complement lysis. IL-10 is capable of inhibiting chemotactic chemotaxis of monocytes. It also significantly affects the further differentiation of monocytes, as it enhances the potential for these cells to eventually differentiate into macrophages, and also allows cells to differentiate into inhibitory APCs while inhibiting myeloid dendritic cell differentiation. IL-10 has little effect on the function of plasma dendritic cells, for example, it only slightly inhibits the production of type I interferons in these cells.