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Desensitization of ...
Desensitization of formyl peptide receptors is abolished in calcium ionophore-primed neutrophils: an association of the ligand-receptor complex to the cytoskeleton is not required for a rapid termination of the NADPH-oxidase response.
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Harbecke, Olle, 1966 (författare)
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- Elwing, Hans-Björne, 1946 (författare)
- Gothenburg University,Göteborgs universitet,Institutionen för cell- och molekylärbiologi,Department of Cell and Molecular Biology
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Follin, P (författare)
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- Karlsson, Anna, 1967 (författare)
- Gothenburg University,Göteborgs universitet,Institutionen för invärtesmedicin, Avdelningen för reumatologi och inflammationsforskning,Institute of Internal Medicine, Dept of Rheumatology and Inflammation Research
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- Dahlgren, Claes, 1949 (författare)
- Gothenburg University,Göteborgs universitet,Institutionen för invärtesmedicin, Avdelningen för reumatologi och inflammationsforskning,Institutionen för medicinsk mikrobiologi och immunologi,Institute of Internal Medicine, Dept of Rheumatology and Inflammation Research,Institute of Medical Microbiology/Immunology
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(creator_code:org_t)
- 1998
- 1998
- Engelska.
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Ingår i: Journal of immunology (Baltimore, Md. : 1950). - 0022-1767. ; 160:5, s. 2463-8
- Relaterad länk:
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https://gup.ub.gu.se...
Abstract
Ämnesord
Stäng
- Binding of ligands to N-formyl peptide chemoattractant receptors exposed on human neutrophils generates signals in the cells that induce an activation of the superoxide anion producing NADPH-oxidase. Ligand binding is followed by a rapid association of the ligand-receptor complex with the cytoskeleton, a process leading to desensitization of the cells with respect to NADPH-oxidase activation. We show that neutrophils that have experienced an intracellular calcium rise obtained through interaction with the calcium-specific ionophore ionomycin are "primed" with respect to the FMLP-induced production of superoxide anions. Mobilization of FMLP receptors from intracellular pools is one well-known mechanism behind the primed response. Based on our finding that ionomycin-treated neutrophils could not be desensitized, we suggest that the lack of association between the ligand-receptor complex and the cytoskeleton is an additional priming mechanism. Since in vivo-exudated neutrophils, which also had mobilized intracellular organelles, could be desensitized, we suggest that the abolished desensitization in ionomycin-treated neutrophils is not due to an inability of newly recruited receptors to couple to the cytoskeleton. We show that a rapid termination of FMLP-induced superoxide anion production is obtained in both desensitizable and nondesensitizable neutrophils, suggesting that the desensitization phenomenon is of limited importance in the oxidase termination process.
Ämnesord
- MEDICIN OCH HÄLSOVETENSKAP -- Medicinska och farmaceutiska grundvetenskaper -- Immunologi inom det medicinska området (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Basic Medicine -- Immunology in the medical area (hsv//eng)
Nyckelord
- Adult
- Cytoplasmic Granules
- enzymology
- metabolism
- Cytoskeleton
- enzymology
- metabolism
- Enzyme Activation
- drug effects
- Humans
- Ionomycin
- pharmacology
- Ligands
- Macromolecular Substances
- N-Formylmethionine Leucyl-Phenylalanine
- blood
- pharmacology
- NADPH Oxidase
- antagonists & inhibitors
- blood
- Neutrophil Activation
- drug effects
- immunology
- Neutrophils
- enzymology
- immunology
- metabolism
- Receptors
- Formyl Peptide
- Receptors
- Immunologic
- blood
- immunology
- metabolism
- Receptors
- Peptide
- blood
- immunology
- metabolism
- Superoxides
- blood
Publikations- och innehållstyp
- ref (ämneskategori)
- art (ämneskategori)
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