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Titolo:
REGULATION OF NEUTROPHIL APOPTOSIS BY TUMOR-NECROSIS-FACTOR-ALPHA - REQUIREMENT FOR TNFR55 AND TNFR75 FOR INDUCTION OF APOPTOSIS IN-VITRO
Autore:
MURRAY J; BARBARA JAJ; DUNKLEY SA; LOPEZ AF; VANOSTADE X; CONDLIFFE AM; DRANSFIELD I; HASLETT C; CHILVERS ER;
Indirizzi:
UNIV EDINBURGH,RIE,DEPT MED,RESP MED UNIT,RAYNE LAB,SCH MED,TEVIOT PLEDINBURGH EH8 9AG MIDLOTHIAN SCOTLAND UNIV EDINBURGH,RIE,DEPT MED,RESP MED UNIT,RAYNE LAB,SCH MED EDINBURGHEH8 9AG MIDLOTHIAN SCOTLAND INST MED & VET SCI,HANSON CTR CANC RES,DIV HUMAN IMMUNOL ADELAIDE SA 5000 AUSTRALIA STATE UNIV GHENT,VIB,LAB MED PROT CHEM B-9000 GHENT BELGIUM
Titolo Testata:
Blood
fascicolo: 7, volume: 90, anno: 1997,
pagine: 2772 - 2783
SICI:
0006-4971(1997)90:7<2772:RONABT>2.0.ZU;2-O
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROGRAMMED CELL-DEATH; COLONY-STIMULATING FACTOR; IN-VITRO; CHEMOTACTIC FACTORS; RESPIRATORY BURST; P55 RECEPTOR; MACROPHAGES; CYTOKINES; SURVIVAL; PHAGOCYTOSIS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
59
Recensione:
Indirizzi per estratti:
Citazione:
J. Murray et al., "REGULATION OF NEUTROPHIL APOPTOSIS BY TUMOR-NECROSIS-FACTOR-ALPHA - REQUIREMENT FOR TNFR55 AND TNFR75 FOR INDUCTION OF APOPTOSIS IN-VITRO", Blood, 90(7), 1997, pp. 2772-2783

Abstract

Granulocyte apoptosis is an important mechanism underlying the removal of redundant neutrophils from an inflammatory focus. The ability of many proinflammatory agents to impede this event suggests that such agents act not only in a priming or secretagogue capacity but also increase neutrophil longevity by delaying apoptosis, We have examined whether this hypothesis holds true for all neutrophil priming agents, in particular tumor necrosis factor-alpha (TNF-alpha), which has been variably reported to either induce, delay, or have no effect on neutrophil apoptosis. After 20 hours coincubation TNF-alpha inhibited neutrophil apoptosis; however, more detailed analysis demonstrated its ability topromote apoptosis in a subpopulation of cells at earlier (2 to 8 hours) times. Formyl-Met-Leu-Phe, platelet-activating factor, inositol hexakisphosphate, lipopolysaccharide, leukotriene B-4, and granulocyte-macrophage colony-stimulating factor all inhibited apoptosis at 6 and 20hours, The early proapoptotic effect of TNF-alpha was concentration-dependent (EC50 2.8 ng/ mt), abolished by TNF-alpha neutralizing antibody, and was not associated with any change in cell viability or recovery. Of relevance to the inflamed site, the ability of TNF-alpha to accelerate apoptosis was lost if neutrophils were primed with 1 mu mol/L PAF or aged for 6 hours before TNF-alpha addition. The TNFR55-selective TNF-alpha mutants (E146K, R32W-S86T) induced neutrophil apoptosis but with a potency 14-fold lower than wild-type TNF-alpha, Although the TNFR75-selective mutant (D143F) did not induce apoptosis, blocking antibodies to both receptor subtypes abolished TNF-alpha-stimulated apoptosis. Hence, TNF-alpha has the unique ability to induce apoptosis in human neutrophils via a mechanism where TNFR75 facilitates the dominantTNFR55 death effect, This may be an important mechanism controlling neutrophil iongevity and clearance in vivo, (C) 1997 by The American Society of Hematology.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 21/01/21 alle ore 04:03:14