IL-10 was first described as a cytokine that is produced by T helper 2 (Th2) cell clones. It inhibits interferon (IFN)-g 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-kB dependent), tumor necrosis factor TNF-a (via TNF receptor p55, NF-kB-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 endotoxinand IFN-g-induced release of IL-1a, IL-6, IL-8, G-CSF, GM-CSF, and TNF-a. In addition, it enhances the production of anti-inflammatory mediators such as IL-1RA and soluble TNFa 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 IFNg-induced cell surface levels of MHC class II, of costimulatory molecules such as CD86 and of some adhesion molecules such as CD58.
原厂资料：
Description:
IL-10 was first described as a cytokine that is produced by T helper 2 (Th2) cell clones. It inhibits interferon (IFN)-g 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-kB dependent), tumor necrosis factor TNF-a (via TNF receptor p55, NF-kB-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 endotoxinand IFN-g-induced release of IL-1a, IL-6, IL-8, G-CSF, GM-CSF, and TNF-a. In addition, it enhances the production of anti-inflammatory mediators such as IL-1RA and soluble TNFa 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 IFNg-induced cell surface levels of MHC class II, of costimulatory molecules such as CD86 and of some adhesion molecules such as CD58.
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