NET amyloidogenic backbone in human activated neutrophils.

摘要: Activated human neutrophils produce a fibrillar DNA network [neutrophil extracellular traps (NETs)] for entrapping and killing bacteria, fungi, protozoa viruses. Our results suggest that the neutrophil show resistant amyloidogenic backbone utilized addressing reputed proteins against non-self. The formation of amyloid fibrils in is regulated by imbalance reactive oxygen species (ROS) cytoplasm. intensity source ROS signal determinant promoting stress-associated responses such as amyloidogenesis closely related events: autophagy, exosome release, activation adrenocorticotrophin hormone/α-melanocyte-stimulating hormone (ACTH/α-MSH) loop synthesis specific cytokines. These interconnected activated neutrophils, have been evaluated from morphofunctional quantitative viewpoint, represent primitive, but potent, innate defence mechanisms. In invertebrates, circulating phagocytic immune cells, when activated, similar to those described previously neutrophils. Invertebrate cells within endoplasmic reticulum cisternae material which then assembled into an scaffold convey melanin close invader. findings, consideration critical role played NET development several pathologies, could explain structural resistance these scaffolds provide basis developing new diagnostic therapeutic approaches immunomediated diseases branch system has pivotal role.