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Role of interleukin-1 and mitogen-activated protein kinases in the mechanisms of action of muramyldipeptide on cells of innate immunity


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Abstract

When you activate glucosaminilmuramildipeptide (Hmtri) gram-negative bacteria, the macrophages produce significantly large quantities of proinflammatory cytokines, particularly tumor necrosis factor (TNF) than dendritic cells (DC), with the same abilities of both types of cells respond to lipopolysaccharide (LPS). Studies have shown that the increased ability of macrophages to respond to Hmtri is not associated with auto - and paracrine mechanisms mediated by cytokines of the family of interleukin-1 (IL-1). At the same time, IL-1a and IL-1β potentiate the response of DC to Hmtri. When comparing macrophages and DCS, activated Hmtri discovered that macrophages have a more pronounced activation of the mitogen-activated protein kinase p38, as well as more prolonged expression of TNF mRNA, all of which, apparently, and determines a more powerful response of macrophages to Hmtri. Thus, new data on the mechanisms of action of muramyldipeptide on cells of innate immunity that could be taken into account in the development and application of muramyldipeptide Immunostimulants and adjuvants.


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