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Christopher Haslett

Researcher at University of Edinburgh

Publications -  217
Citations -  27659

Christopher Haslett is an academic researcher from University of Edinburgh. The author has contributed to research in topics: Inflammation & Apoptosis. The author has an hindex of 79, co-authored 216 publications receiving 26272 citations. Previous affiliations of Christopher Haslett include Queen's University & Medical Research Council.

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A blast from the past: clearance of apoptotic cells regulates immune responses

TL;DR: Apoptosis, which is a programmed and physiological form of cell death, is known to shape the immune system by regulating populations of effector lymphocytes, but the binding and ingestion of dying cells by monocytes/macrophages and dendritic cells can also influence immune responses markedly by enhancing or suppressing inflammation.
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Macrophage phagocytosis of aging neutrophils in inflammation. Programmed cell death in the neutrophil leads to its recognition by macrophages.

TL;DR: Changes in the senescent neutrophil that are associated with their recognition by macrophages are the subject of this investigation, and these processes may represent a mechanism for the removal of neutrophils during inflammation that also serves to limit the degree of tissue injury.
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Resolution of inflammation: state of the art, definitions and terms.

TL;DR: A consensus report was needed that addresses the rapid progress in this emerging field and details how the specific study of resolution of acute inflammation provides leads for novel anti‐inflammatory therapeutics, as well as defines the terms and key components of interest in the resolution process within tissues as appreciated today.
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Phagocyte recognition of cells undergoing apoptosis

TL;DR: Recent data indicate that phagocyte recognition of apoptotic cells as 'senescent-self' involves at least three classes of receptors on the phagocytes surface, while apoptotic Cells may display their 'edible' status in a number of different ways.
Journal Article

Modulation of multiple neutrophil functions by preparative methods or trace concentrations of bacterial lipopolysaccharide.

TL;DR: The effects of trace concentrations of LPS in the modulation of neutrophil function may have relevance to the pathophysiology of endotoxemia and its resultant tissue injury.