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Aggregated neutrophil extracellular traps limit inflammation by degrading cytokines and chemokines
It is reported that neutrophils recruited to sites of inflammation undergo oxidative burst and form neutrophil extracellular traps (NETs), and aggregated NETs promote the resolution of neutrophilic inflammation by degrading cytokines and chemokines and disrupting neutrophIL recruitment and activation. Expand
To NET or not to NET:current opinions and state of the science regarding the formation of neutrophil extracellular traps
Since the discovery and definition of neutrophil extracellular traps (NETs) 14 years ago, numerous characteristics and physiological functions of NETs have been uncovered. Nowadays, the fieldExpand
Host DNases prevent vascular occlusion by neutrophil extracellular traps
A noncanonical mechanism for vascular occlusion based on neutrophil extracellular traps (NETs), DNA fibers released by neutrophils during inflammation are reported and provide dual host protection against deleterious effects of intravascular NETs. Expand
Mitochondrial dynamics during cell cycling
How vital proper functioning of mitochondria is in maintaining cell integrity and preventing carcinogenesis is indicated by several proteins change in activity and might link the mitochondrial fission/fusion events with processes such as alteration of mitochondrial membrane potential, apoptosis, necrosis, cell cycle arrest, and malignant growth. Expand
Decrease of sialic acid residues as an eat-me signal on the surface of apoptotic lymphocytes
These findings support the importance of the glycocalyx, notably the terminal sialic acids, in the regulation of apoptotic cell clearance, and suggest changes in surface glycosylation can either directly mediate cellular engulfment or enhance phagocytosis by cooperation with further engulfment signals. Expand
Lectinocytochemical detection of apoptotic murine leukemia L1210 cells
  • R. Bilyy, R. Stoika
  • Biology, Medicine
  • Cytometry. Part A : the journal of the…
  • 1 December 2003
This work investigated whether specific changes in the expression of plasma membrane glycoproteins take place during apoptosis and whether these changes could be used for a quantitative estimation of apoptosis. Expand
Cytotoxicity of crystals involves RIPK3-MLKL-mediated necroptosis
Crystals cause injury in numerous disorders, and induce inflammation via the NLRP3 inflammasome, however, it remains unclear how crystals induce cell death. Here we report that crystals of calciumExpand
The Pathogenicity of Anti-β2GP1-IgG Autoantibodies Depends on Fc Glycosylation
It is concluded that the increased sialylation of anti-β2GP1-IgG of sera of healthy individuals limits their pathogenicity. Expand
Second generation of thiazolylmannosides, FimH antagonists for E. coli-induced Crohn's disease.
A second generation of TazMans is developed with improved chemical stability and the identification of a candidate for further in vivo evaluations of E. coli strains implied in the gut inflammation of patients with Crohn's disease. Expand
Blood-borne phagocytes internalize urate microaggregates and prevent intravascular NETosis by urate crystals
It is reported that complement proteins and fetuins facilitate the continuous clearance by blood-borne phagocytes and resident macrophages of small urate microaggregates (UMA) that initially form in hyperuricemic blood. Expand