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Prepublished online as a Blood First Edition Paper on October 10, 2002; DOI 10.1182/blood-2002-02-0522. This Article Full Text Full Text (PDF) All Versions of this Article: 2002-02-0522v1 101/5/1987    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Maianski, N. A. Articles by Kuijpers, T. W. Search for Related Content PubMed PubMed Citation Articles by Maianski, N. A. Articles by Kuijpers, T. W. Related Collections Phagocytes Apoptosis Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 1 March 2003, Vol. 101, No. 5, pp. 1987-1995 PHAGOCYTES Tumor necrosis factor  induces a caspase-independent death pathway in human neutrophils Nikolai A. Maianski, Dirk Roos, and Taco W. Kuijpers From the Sanquin Research at Central Laboratory of the Netherlands Blood Transfusion Service, Landsteiner Laboratory, and Emma Children's Hospital, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands; and Medical Academy, Nizhniy Novgorod, Russia. Tumor necrosis factor  (TNF-) is a cytokine with multiple roles in the immune system, including the induction and potentiation of cellular functions in neutrophils (PMNs). TNF- also induces apoptotic signals leading to the activation of several caspases, which are involved in different steps of the process of cell death. Inhibition of caspases usually increases cell survival. Here, we found that inhibition of caspases by the general caspase inhibitor zVAD-fmk did not prevent TNF--induced PMN death. After 6 hours of incubation, TNF- alone caused PMN death with characteristic apoptotic features (typical morphologic changes, DNA laddering, external phosphatidyl serine [PS] exposure in the plasma membrane, Bax clustering and translocation to the mitochondria, and degradation of mitochondria), which coincided with activation of caspase-8 and caspase-3. However, in the presence of TNF-, PMNs died even when caspases were completely inhibited. This type of cell death lacked nuclear features of apoptosis (ie, no DNA laddering but aberrant hyperlobulated nuclei without typical chromatin condensation) and demonstrated no Bax redistribution, but it did show mitochondria clustering and plasma membrane PS exposure. In contrast, Fas-triggered PMN apoptosis was completely blocked by zVAD-fmk. Experiments with scavengers of reactive oxygen species (ROS) and with inhibitors of mitochondrial respiration, with PMN-derived cytoplasts (which lack mitochondria) and with PMNs from patients with chronic granulomatous disease (which have impaired nicotinamide adenine dinucleotide phosphate [NADPH] oxidase) indicated that TNF-/zVAD-fmk-induced cell death depends on mitochondria-derived ROS. Thus, TNF- can induce a "classical," caspase-dependent and a "nonclassical" caspase-independent cell death. © 2003 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: S. Moriceau, C. Kantari, J. Mocek, N. Davezac, J. Gabillet, I. C. Guerrera, F. Brouillard, D. Tondelier, I. Sermet-Gaudelus, C. Danel, et al. Coronin-1 Is Associated with Neutrophil Survival and Is Cleaved during Apoptosis: Potential Implication in Neutrophils from Cystic Fibrosis Patients J. 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