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The humoral pattern recognition receptor PTX3 is stored in neutrophil granules and localizes in extracellular traps

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TLDR
The long pentraxin (PTX) 3 is produced by macrophages and myeloid dendritic cells in response to Toll-like receptor agonists and represents a nonredundant component of humoral innate immunity against selected pathogens.
Abstract
The long pentraxin (PTX) 3 is produced by macrophages and myeloid dendritic cells in response to Toll-like receptor agonists and represents a nonredundant component of humoral innate immunity against selected pathogens. We report that, unexpectedly, PTX3 is stored in specific granules and undergoes release in response to microbial recognition and inflammatory signals. Released PTX3 can partially localize in neutrophil extracellular traps formed by extruded DNA. Eosinophils and basophils do not contain preformed PTX3. PTX3-deficient neutrophils have defective microbial recognition and phagocytosis, and PTX3 is nonredundant for neutrophil-mediated resistance against Aspergillus fumigatus. Thus, neutrophils serve as a reservoir, ready for rapid release, of the long PTX3, a key component of humoral innate immunity with opsonic activity.

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Neutrophils in the activation and regulation of innate and adaptive immunity

TL;DR: Neutrophils have long been viewed as the final effector cells of an acute inflammatory response, with a primary role in the clearance of extracellular pathogens, but more recent evidence has extended the functions of these cells.
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Neutrophil Extracellular Traps Contain Calprotectin, a Cytosolic Protein Complex Involved in Host Defense against Candida albicans

TL;DR: The present investigations confirmed the antifungal activity of calprotectin in vitro and demonstrated that it contributes to effective host defense against C. albicans in vivo.
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Thrombosis as an intravascular effector of innate immunity

TL;DR: Recent work suggesting that thrombosis under certain circumstances has a major physiological role in immune defence is summarized, and the term immunothromBosis is introduced to describe this process.
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Neutrophils, from marrow to microbes.

TL;DR: Neutrophils are produced in the bone marrow from stem cells that proliferate and differentiate to mature neutrophils fully equipped with an armory of granules that contain proteins that enable the neutrophil to deliver lethal hits against microorganisms, but also to cause great tissue damage.
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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.
References
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Journal ArticleDOI

Innate Immune Recognition

TL;DR: Microbial recognition by Toll-like receptors helps to direct adaptive immune responses to antigens derived from microbial pathogens to distinguish infectious nonself from noninfectious self.
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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.
Journal ArticleDOI

The acute phase response

TL;DR: This review outlines the principal cellular and molecular mechanisms that control initiation of the tissue response at the site of injury, the recruitment of the systemic defense mechanisms, the acute phase response of the liver and the resolution of the acutephase response.
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Neutrophils and immunity: challenges and opportunities.

TL;DR: Neutrophils inform and shape immune responses, contribute to the repair of tissue as well as its breakdown, use killing mechanisms that enrich the concepts of specificity, and offer exciting opportunities for the treatment of neoplastic, autoinflammatory and autoimmune disorders.
Journal ArticleDOI

How neutrophils kill microbes

TL;DR: Killing was previously believed to be accomplished by oxygen free radicals and other reactive oxygen species generated by the NADPH oxidase, and by oxidized halides produced by myeloperoxidase, but this is incorrect.
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