Regulation of Neutrophil Apoptosis by Tumor Necrosis Factor-α: Requirement for TNFR55 and TNFR75 for Induction of Apoptosis In Vitro
Joanna Murray,Joanna Murray,Joanna Murray,Jeffrey A.J. Barbara,Jeffrey A.J. Barbara,Jeffrey A.J. Barbara,Sarah A. Dunkley,Sarah A. Dunkley,Sarah A. Dunkley,Angel F. Lopez,Angel F. Lopez,Angel F. Lopez,Xaveer Van Ostade,Xaveer Van Ostade,Xaveer Van Ostade,Alison M. Condliffe,Alison M. Condliffe,Alison M. Condliffe,Ian Dransfield,Christopher Haslett,Edwin R. Chilvers,Edwin R. Chilvers,Edwin R. Chilvers +22 more
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TLDR
TNF-alpha has the unique ability to induce apoptosis in human neutrophils via a mechanism where TNFR75 facilitates the dominant TNFR55 death effect, and may be an important mechanism controlling neutrophil longevity and clearance in vivo.About:
This article is published in Blood.The article was published on 1997-10-01 and is currently open access. It has received 312 citations till now. The article focuses on the topics: Programmed cell death & Granulocyte.read more
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Neutrophil function in inflammation and inflammatory diseases
TL;DR: Drugs already used to treat RA down-regulate many neutrophil functions, including migration to the joint, degranulation and production of inflammatory mediators, and these cells should be considered as important targets for the development of new therapies in the future.
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TNF receptor subtype signalling: differences and cellular consequences.
TL;DR: This review addresses the structural basis of TNF signalling, the pathways employed with their cellular consequences, and focuses on the specific role played by each of the two TNF receptor isotypes, TNFR1 and TNFR2.
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Granulocyte apoptosis and its role in the resolution and control of lung inflammation.
TL;DR: Although it had been assumed that extravasated neutrophils disintegrated (undergo necrosis) in situ, this work has demonstrated an alternative fate, whereby the cell undergoes apoptosis, a process that has different implications for the control of inflammation.
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Molecular control of neutrophil apoptosis.
TL;DR: This review summarises current knowledge on the molecular mechanisms and components of neutrophil apoptosis.
Journal ArticleDOI
TNF-induced signaling in apoptosis.
TL;DR: Out of the almost 17 members of the TNF superfamily, TNF is probably the most potent inducer of apoptosis, which activates both cell-survival and cell-death mechanisms simultaneously.
References
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A rapid and simple method for measuring thymocyte apoptosis by propidium iodide staining and flow cytometry
TL;DR: A flow cytometric method for measuring the percentage of apoptotic nuclei after propidium iodide staining in hypotonic buffer is developed and shown an excellent correlation with the results obtained with both electrophoretic and colorimetric methods.
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Programmed cell death induced by ceramide
TL;DR: The effects of C2-ceramide on DNA fragmentation were prevented by the protein kinase C activator phorbol 12-myristate 13-acetate, which suggests the existence of two opposing intracellular pathways in the regulation of apoptosis.
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Macrophage phagocytosis of aging neutrophils in inflammation. Programmed cell death in the neutrophil leads to its recognition by macrophages.
John Savill,Andrew H. Wyllie,Janet E. Henson,Mark Walport,Peter M. Henson,Christopher Haslett +5 more
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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A novel domain within the 55 kd TNF receptor signals cell death.
TL;DR: Alanine-scanning mutagenesis of TNF-R1 confirmed that many of the amino acids conserved with Fas antigen are critical for the cytotoxic signal and is likely to define a novel domain (death domain) that signals programmed cell death.
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Modulation of granulocyte survival and programmed cell death by cytokines and bacterial products
TL;DR: Prolongation of survival may be important for the regulation of host resistance and inflammation, and may represent a crucial permissive step for certain cytokines and microbial products that activate gene expression and function in PMN.