2020
DOI: 10.1007/s13770-020-00241-z
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Extracellular Trap by Blood Cells: Clinical Implications

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Cited by 33 publications
(27 citation statements)
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“…10,11 Increased NET formation is well known in various clinical conditions, including sepsis, trauma, autoimmune diseases, deep vein thrombosis, atherosclerosis, and thrombotic microangiopathy. 12,13 Because multiple nosologies share humoral and cellular activation pathways, we asked whether TAVI increases circulating soluble suppression of tumorigenicity-2 (sST2) and its counterpart interleukin (IL)-33, a known biological alarmin that would serve as an additional biological marker for ongoing inflammatory processes. [14][15][16] In this study, we investigated for the first time whether BHVs employed for TAVI augment an a-Gal-specific humoral immune response of total immunoglobulin (Ig) G, IgG subclasses, and IgE; activate the complement system via C3a; induce citrullinated H3 (CitH3) as a marker for NET formation; and initiate the IL-33/ST2 pathway within 90 days after intervention compared with baseline levels.…”
Section: Central Messagementioning
confidence: 99%
“…10,11 Increased NET formation is well known in various clinical conditions, including sepsis, trauma, autoimmune diseases, deep vein thrombosis, atherosclerosis, and thrombotic microangiopathy. 12,13 Because multiple nosologies share humoral and cellular activation pathways, we asked whether TAVI increases circulating soluble suppression of tumorigenicity-2 (sST2) and its counterpart interleukin (IL)-33, a known biological alarmin that would serve as an additional biological marker for ongoing inflammatory processes. [14][15][16] In this study, we investigated for the first time whether BHVs employed for TAVI augment an a-Gal-specific humoral immune response of total immunoglobulin (Ig) G, IgG subclasses, and IgE; activate the complement system via C3a; induce citrullinated H3 (CitH3) as a marker for NET formation; and initiate the IL-33/ST2 pathway within 90 days after intervention compared with baseline levels.…”
Section: Central Messagementioning
confidence: 99%
“…ETs in MCs are known as MCETs (mast cell extracellular traps). The presence of MCETs in vitro related to various infections caused by bacteria, protozoa, fungi, and also in other pathological conditions has already been described [163]. MCETs are comprised of nuclear DNA, tryptase, histones, and cathelicidins.…”
Section: Mast Cellsmentioning
confidence: 92%
“…In humans, cathelicidin LL-37 has already been identified, as well as cathelicidin-related AMP (CRAMP) in mice [164]. Typically, the formation of MCETs is ROS-dependent [163], and MCs undergo nuclear membrane rupture and subsequently cell death [33].…”
Section: Mast Cellsmentioning
confidence: 99%
“…ETs are produced not only by neutrophils, but also by other immune cell types, such as monocytes and macrophages, eosinophils, basophils, and mast cells [ 7 , 8 ]. In addition to the presence of DNA, they contain associated molecules that can be specific depending on the cell type and on the stimuli [ 9 ]. Although ETs play a beneficial role in host defences, they consist of a filamentous network of chromosomal and/or mitochondrial DNA released from the cell after the breakdown of the nuclear/mitochondrial membrane, usually leading to suicidal death, distinct from apoptosis or necrosis (reviewed in References [ 2 , 10 ]).…”
Section: Extracellular Traps (Etosis)mentioning
confidence: 99%