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Open AccessJournal ArticleDOI

Neutrophil extracellular traps mediate a host defense response to human immunodeficiency virus-1.

TLDR
It is shown that NETs capture human immunodeficiency virus (HIV)-1 and promote HIV-1 elimination through myeloperoxidase and α-defensin and that NET formation is an antiviral response that is counteracted by HIV- 1.
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This article is published in Cell Host & Microbe.The article was published on 2012-07-19 and is currently open access. It has received 557 citations till now. The article focuses on the topics: Neutrophil extracellular traps & Myeloperoxidase.

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Citations
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Neutrophil recruitment and function in health and inflammation

TL;DR: The key features of the life of a neutrophil are discussed, from its release from bone marrow to its death, and the mechanisms that are used by neutrophils to promote protective or pathological immune responses at different sites are explained.
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Neutrophil extracellular traps in immunity and disease

TL;DR: The identification of molecules that modulate the release of NETs has helped to refine the view of the role of neutrophils in immune protection, inflammatory and autoimmune diseases and cancer.
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Neutrophil Extracellular Traps: Double-Edged Swords of Innate Immunity

TL;DR: Experimental evidence suggests that neutrophil extracellular traps participate in pathogenesis of autoimmune and inflammatory disorders, with proposed involvement in glomerulonephritis, chronic lung disease, sepsis, and vascular disorders.
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Neutrophil extracellular traps: Is immunity the second function of chromatin?

TL;DR: The understanding of how NETs are made, their function in infections and as danger signals, and their emerging importance in autoimmunity and coagulation are reviewed.
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Neutrophils sense microbe size and selectively release neutrophil extracellular traps in response to large pathogens

TL;DR: It is found that neutrophils sensed microbe size and selectively released neutrophil extracellular traps (NETs) in response to large pathogens, such as Candida albicans hyphae andextracellular aggregates of Mycobacterium bovis, but not inresponse to small yeast or single bacteria.
References
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Neutrophil extracellular traps kill bacteria

TL;DR: It is described that, upon activation, neutrophils release granule proteins and chromatin that together form extracellular fibers that bind Gram-positive and -negative bacteria, which degrade virulence factors and kill bacteria.
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Species-Specific Recognition of Single-Stranded RNA via Toll-like Receptor 7 and 8

TL;DR: It is shown that guanosine (G)- and uridine (U)-rich ssRNA oligonucleotides derived from human immunodeficiency virus–1 (HIV-1) stimulate dendritic cells and macrophages to secrete interferon-α and proinflammatory, as well as regulatory, cytokines, and these data suggest that ssRNA represents a physiological ligand for TLR7 and TLR8.
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Novel cell death program leads to neutrophil extracellular traps

TL;DR: This novel ROS-dependent death allows neutrophils to fulfill their antimicrobial function, even beyond their lifespan.
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DC-SIGN, a dendritic cell-specific HIV-1-binding protein that enhances trans-infection of T cells

TL;DR: It is proposed that DC-SIGN efficiently captures HIV-1 in the periphery and facilitates its transport to secondary lymphoid organs rich in T cells, to enhance infection in trans of these target cells.
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The roles of TLRs, RLRs and NLRs in pathogen recognition

TL;DR: Recent insights into pathogen sensing by PRRs are summarized and specific signaling pathways that lead to expression of genes that tailor immune responses to particular microbes are summarized.
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