چاپ صفحه |  صفحه نخست سامانه |  نویسندگان |  اطلاعات تفضیلی |  دانلود مقاله | دانشگاه علوم پزشکی تبریز |
| نویسنده | نفر چندم مقاله |
|---|---|
| سارا سجادی | اول |
| عنوان | متن |
|---|---|
| کلمات کلیدی | NETosis; Autoimmune; Inflammation; Neutrophil |
| خلاصه مقاله | NETosis is the process of NETs (Neutrophil extracellular traps) production which includes three parts: DNA and histones as nuclear components, myeloperoxidase (MPO), cathepsin C, and neutrophil elastase (NE) as granule components, and catalase as cytoplasm compound. The excessive formation and release of NETs can trigger a variety of autoimmune diseases. The count of low-density neutrophils (LDN) increased in NETosis. These cells have a key role in dendritic cell activation through TLR9. This phenomenon results in antigen presentation to B-cells, interferon response, and the release of pro-inflammatory cytokines. The level of calcium ions increases in the cytoplasm. NOX2 enzymes assemble through the activation of the PKC pathway and O2- ions are produced which induce H+ entrance to the phagosome. Consequently, H2O2 is generated as reactive oxygen species (ROS). Histones are hyper-citrullinated by the activation of Peptidylarginine deiminases (PAD2 and 4). Correspondingly, some inflammatory cytokines (like IL1 and IL36) can activate NE which causes histone degradation. Hyper-citrullinated histones prevent histone methylation and promote B-cells to produce ACPA. IL6 and TNF-α activate platelets and induce endothelial cell damage. Therefore, ROS production and chromatin unfolding are the two main biochemical events that occur during NETosis and amplify autoimmune disease by inhibiting apoptosis, inactivation of tyrosine phosphatase, and p38 stimulation. |
| نام فایل | تاریخ درج فایل | اندازه فایل | دانلود |
|---|---|---|---|
| Abstract.pdf | 1403/06/17 | 112483 | دانلود |
| poster ICIA 2023.pdf | 1403/06/17 | 253364 | دانلود |
