Recombinant human IL-10 (ELISA Std.)

IL-10 was first described as a cytokine that is produced by T helper 2 (Th2) cell clones. It inhibits interferon (IFN)-gamma synthesis in Th1 cell, and therefore it was initially called cytokine synthesis inhibiting factor (CSIF). Macrophages are the main source of IL-10 and its secretion can be stimulated by endotoxin (via Toll-like receptor 4, NF-kappaB dependent), tumor necrosis factor TNF-alpha (via TNF receptor p55, NF-kappaB-dependent), catecholamines, and IL-1. IL-10 controls inflammatory processes by suppressing the expression of proinflammatory cytokines, chemokines, adhesion molecules, as well as antigen-presenting and costimulatory molecules in monocytes/macrophages, neutrophils, and T cells. IL-10 inhibits the production of proinflammatory mediators by monocytes and macrophages such as endotoxin- and IFN-gamma-induced release of IL-1alpha, IL-6, IL-8, G-CSF, GM-CSF, and TNF-alpha. In addition, it enhances the production of anti-inflammatory mediators such as IL-1RA and soluble TNFalpha receptors. IL-10 inhibits the capacity of monocytes and macrophages to present antigen to T cells. This is realized by down-regulation of constitutive and IFNgamma-induced cell surface levels of MHC class II, of costimulatory molecules such as CD86 and of some adhesion molecules such as CD58.