Neutrophil extracellular traps mediate a host defense response to human immunodeficiency virus-1.
By T. Saitoh, J. Komano, Yasunori Saitoh, Takuma Misawa, Michihiro Takahama, Tatsuya Kozaki, Takuya Uehata, Hidenori Iwasaki, Hiroko Omori, S. Yamaoka and 2 more. Cell Host and Microbe, 2012
698 citations recorded by the source corpus.
Subfields: Immunology
View Paper: https://www.semanticscholar.org/paper/a117272d0bfecb4c1ebdce21b26552cb6a5d6ccc
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In Immunology
Citations in the corpus
- Thrombosis: tangled up in NETs. (2014, background): “NETsalsohave the ability to trap andkill fungi,(3) are released in viral infections,(4) and can sequester viruses.(5) Interestingly, this ability of the host to release extracellular traps to protect itself from pathogens is evolutionarily conserved in plants, with root border cells secreting extrac”
- Mucosal Immunity in the Female Genital Tract, HIV/AIDS (2014, background): “Recently, Neutrophil extracellular traps (NETs) have been described as a host defense response to human immunodeficiency virus-1 preventing virus spreading [162].”
- Neutrophil cell surface receptors and their intracellular signal transduction pathways (2013, neutral): “[224]).”
- Diverse novel functions of neutrophils in immunity, inflammation, and beyond (2013, background): “In a recent study, Saitoh et al. (2012) proposed a role for NETs in the control of HIV-1 infection.”
- NETosis: how vital is it? (2013, methodology): “On the other hand, Saitoh et al also visualized large sheets of DNA in vitro using superresolution microscopy.(74)”
- Neutrophil extracellular traps (NETs): Double-edged swords of innate immunity (2012, background): “This virus can develop an anti-NET response mediated by IL-10 (56).”
- Neutrophil Extracellular Traps and Its Implications in Inflammation: An Overview (2017, background): “Staphylococcos aureus Leukotoxin GH and Panton– Valentine leucocidin Osteomyelitis, endocarditis, bacteremia, and gastroenteritis Reactive oxygen species (ROS)-independent induction with nuclear DNA liberation, toll-like receptor (TLR)2, and C3 dependent Vital (14, 27) Streptococcus pneumoniae EndA ”