Serveur d'exploration Chloroquine

Attention, ce site est en cours de développement !
Attention, site généré par des moyens informatiques à partir de corpus bruts.
Les informations ne sont donc pas validées.

The mechanisms of action of disease-modifying antirheumatic drugs: A review with emphasis on macrophage signal transduction and the induction of proinflammatory cytokines

Identifieur interne : 002857 ( Main/Exploration ); précédent : 002856; suivant : 002858

The mechanisms of action of disease-modifying antirheumatic drugs: A review with emphasis on macrophage signal transduction and the induction of proinflammatory cytokines

Auteurs : Jan Bondeson

Source :

RBID : ISTEX:A6340C83C30596512B99FDF4B12F6E39C5A55E13

English descriptors

Abstract

Abstract: 1. 1. Rheumatoid arthritis (RA) is probably the most common source of treatable disability. A major problem in modern rheumatology is that the mechanism(s) of action of the currently used disease-modifying antirheumatic drugs (DMARDs) remain unclear. Many of these drugs entered rheumatology mainly through clinical intuition and have been used for decades. 2. 2. The former T-cell-centered paradigm of rheumatoid inflammation has given way to a model of inflammation highlighting the macrophage and its proinflammatory cytokines. In particular, tumor necrosis factor α (TNF-α) has gained prominence as a central proinflammatory mediator in RA, and antibodies against TNF-α have been successfully used in patients with RA. 3. 3. This review will summarize the recent advances in determining the mechanisms of action of the currently used DMARDs, with particular emphasis on their effects on the induction of TNF-α and interleukin 1 (IL-1) in mononuclear phagocytes. Although some DMARDs, such as auranofin, antimalarials and tenidap, act as inhibitors of the induction of these cytokines in monocytes or macrophages or both, other drugs, such as methotrexate, D-penicillamine and aurothiomalate, do not seem to affect either TNF-α or IL-1. 4. 4. The drugs' effects on proinflammatory cytokine induction are correlated to those on other macrophage responses.

Url:
DOI: 10.1016/S0306-3623(96)00419-3


Affiliations:


Links toward previous steps (curation, corpus...)


Le document en format XML

<record>
<TEI wicri:istexFullTextTei="biblStruct">
<teiHeader>
<fileDesc>
<titleStmt>
<title>The mechanisms of action of disease-modifying antirheumatic drugs: A review with emphasis on macrophage signal transduction and the induction of proinflammatory cytokines</title>
<author>
<name sortKey="Bondeson, Jan" sort="Bondeson, Jan" uniqKey="Bondeson J" first="Jan" last="Bondeson">Jan Bondeson</name>
</author>
</titleStmt>
<publicationStmt>
<idno type="wicri:source">ISTEX</idno>
<idno type="RBID">ISTEX:A6340C83C30596512B99FDF4B12F6E39C5A55E13</idno>
<date when="1997" year="1997">1997</date>
<idno type="doi">10.1016/S0306-3623(96)00419-3</idno>
<idno type="url">https://api.istex.fr/ark:/67375/6H6-VXN65VDF-4/fulltext.pdf</idno>
<idno type="wicri:Area/Istex/Corpus">000084</idno>
<idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">000084</idno>
<idno type="wicri:Area/Istex/Curation">000084</idno>
<idno type="wicri:Area/Istex/Checkpoint">001650</idno>
<idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Checkpoint">001650</idno>
<idno type="wicri:doubleKey">0306-3623:1997:Bondeson J:the:mechanisms:of</idno>
<idno type="wicri:Area/Main/Merge">002906</idno>
<idno type="wicri:Area/Main/Curation">002857</idno>
<idno type="wicri:Area/Main/Exploration">002857</idno>
</publicationStmt>
<sourceDesc>
<biblStruct>
<analytic>
<title level="a">The mechanisms of action of disease-modifying antirheumatic drugs: A review with emphasis on macrophage signal transduction and the induction of proinflammatory cytokines</title>
<author>
<name sortKey="Bondeson, Jan" sort="Bondeson, Jan" uniqKey="Bondeson J" first="Jan" last="Bondeson">Jan Bondeson</name>
<affiliation>
<wicri:noCountry code="subField">0181-3834499]</wicri:noCountry>
</affiliation>
</author>
</analytic>
<monogr></monogr>
<series>
<title level="j">General Pharmacology</title>
<title level="j" type="abbrev">GPH</title>
<idno type="ISSN">0306-3623</idno>
<imprint>
<publisher>ELSEVIER</publisher>
<date type="published" when="1997">1997</date>
<biblScope unit="volume">29</biblScope>
<biblScope unit="issue">2</biblScope>
<biblScope unit="page" from="127">127</biblScope>
<biblScope unit="page" to="150">150</biblScope>
</imprint>
<idno type="ISSN">0306-3623</idno>
</series>
</biblStruct>
</sourceDesc>
<seriesStmt>
<idno type="ISSN">0306-3623</idno>
</seriesStmt>
</fileDesc>
<profileDesc>
<textClass>
<keywords scheme="Teeft" xml:lang="en">
<term>Activation</term>
<term>Activator</term>
<term>Acute phase reactants</term>
<term>Agents actions</term>
<term>Antimalarial</term>
<term>Antimalarial compounds</term>
<term>Antirheumatic</term>
<term>Antirheumatic drugs</term>
<term>Antirheumatic gold compounds</term>
<term>Arachidonate</term>
<term>Arachidonate release</term>
<term>Arachidonic</term>
<term>Arachidonic acid</term>
<term>Arend</term>
<term>Arthritis</term>
<term>Arthritis rheum</term>
<term>Articular</term>
<term>Assay</term>
<term>Auranofin</term>
<term>Aurothioglucose</term>
<term>Aurothiomalate</term>
<term>Azathioprine</term>
<term>Betts</term>
<term>Bimodal effect</term>
<term>Bioassay</term>
<term>Biochem</term>
<term>Biol</term>
<term>Biophys</term>
<term>Blood monocytes</term>
<term>Bondeson</term>
<term>Calcium ionophore</term>
<term>Cartilage</term>
<term>Cartilage destruction</term>
<term>Cascade</term>
<term>Cell membrane</term>
<term>Cell types</term>
<term>Chang</term>
<term>Chem</term>
<term>Chemotaxis</term>
<term>Chloroquine</term>
<term>Clin</term>
<term>Clinical intuition</term>
<term>Clinical response</term>
<term>Clinical studies</term>
<term>Compound</term>
<term>Cyclooxygenase</term>
<term>Cyclooxygenase inhibition</term>
<term>Cyclosporin</term>
<term>Cytokine</term>
<term>Cytokine production</term>
<term>Danis</term>
<term>Dayer</term>
<term>Diacylglycerol</term>
<term>Dinarello</term>
<term>Disease activity</term>
<term>Dmards</term>
<term>Duff</term>
<term>Eicosanoid</term>
<term>Eicosanoid formation</term>
<term>Elisa</term>
<term>Elisa study</term>
<term>Endothelial cells</term>
<term>Epidermal</term>
<term>Epidermal growth factor</term>
<term>Ester</term>
<term>Febs lett</term>
<term>Feldmann</term>
<term>Felson</term>
<term>Fibroblast</term>
<term>Froscio</term>
<term>Gold complexes</term>
<term>Gold compound</term>
<term>Gold compounds</term>
<term>Gold sodium thiomalate</term>
<term>Growth factor</term>
<term>Human blood monocytes</term>
<term>Human macrophages</term>
<term>Human monocytes</term>
<term>Human neutrophils</term>
<term>Human synovial cells</term>
<term>Hurst</term>
<term>Hydrophilic gold compounds</term>
<term>Hydroxychloroquine</term>
<term>Immunol</term>
<term>Important role</term>
<term>Inducer</term>
<term>Induction</term>
<term>Inflammation</term>
<term>Inflammatory</term>
<term>Inflammatory cells</term>
<term>Inhibition</term>
<term>Inhibitor</term>
<term>Inhibitory</term>
<term>Inhibitory effect</term>
<term>Inositol</term>
<term>Interleukin</term>
<term>Intracellular</term>
<term>Isoenzymes</term>
<term>Joint destruction</term>
<term>Kinase</term>
<term>Leukocyte</term>
<term>Leukocyte biol</term>
<term>Leukotriene</term>
<term>Liposomal methotrexate</term>
<term>Lipoxygenase</term>
<term>Lipoxygenase metabolites</term>
<term>Lipoxygenase pathways</term>
<term>Lipoxygenase products</term>
<term>Lund university</term>
<term>Lysosomal</term>
<term>Macrophage</term>
<term>Macrophage arachidonate release</term>
<term>Macrophage signal transduction</term>
<term>Maini</term>
<term>Many rheumatologists</term>
<term>Matsubara</term>
<term>Mediator</term>
<term>Metabolism</term>
<term>Methotrexate</term>
<term>Monoclonal antibodies</term>
<term>Monocyte</term>
<term>Monocyte chemoattractant protein</term>
<term>Mononuclear</term>
<term>Mononuclear cells</term>
<term>Mononuclear phagocytes</term>
<term>Mouse macrophages</term>
<term>Mrna</term>
<term>Mrna level</term>
<term>Murine</term>
<term>Necrosis</term>
<term>Neutrophil</term>
<term>Neutrophil chemotaxis</term>
<term>Nielsen</term>
<term>Nsaid</term>
<term>Other studies</term>
<term>Other transcription factors</term>
<term>Parente</term>
<term>Particular interest</term>
<term>Pathway</term>
<term>Peripheral blood</term>
<term>Peripheral blood monocytes</term>
<term>Peritoneal macrophages</term>
<term>Phagocyte</term>
<term>Pharmac</term>
<term>Phorbol</term>
<term>Phorbol ester</term>
<term>Phospholipase</term>
<term>Phospholipid</term>
<term>Phosphorylate</term>
<term>Phosphorylated</term>
<term>Phosphorylation</term>
<term>Pivotal</term>
<term>Pivotal role</term>
<term>Placebo</term>
<term>Platelet</term>
<term>Potent inhibitor</term>
<term>Potentiating effect</term>
<term>Proinflammatory</term>
<term>Proinflammatory cytokines</term>
<term>Prostaglandin</term>
<term>Prostanoid</term>
<term>Prostanoid formation</term>
<term>Prostanoid synthesis</term>
<term>Protein</term>
<term>Protein kinase</term>
<term>Protein kinases</term>
<term>Quinacrine</term>
<term>Receptor</term>
<term>Receptor antagonist</term>
<term>Receptor tyrosine kinase</term>
<term>Receptor tyrosine kinases</term>
<term>Rheum</term>
<term>Rheumatic diseases</term>
<term>Rheumatoid</term>
<term>Rheumatoid arthritis</term>
<term>Rheumatoid arthritis patients</term>
<term>Rheumatoid inflammation</term>
<term>Rheumatoid synovial fluid</term>
<term>Rheumatol</term>
<term>Rheumatology</term>
<term>Scand</term>
<term>Serum levels</term>
<term>Several studies</term>
<term>Side effects</term>
<term>Signal transduction</term>
<term>Similar concentrations</term>
<term>Soluble receptor</term>
<term>Stimulatory effect</term>
<term>Sulfapyridine</term>
<term>Sulfasalazine</term>
<term>Sulphasalazine</term>
<term>Sundler</term>
<term>Superoxide</term>
<term>Symons</term>
<term>Synovial</term>
<term>Synovial cells</term>
<term>Synovial fluid</term>
<term>Target cells</term>
<term>Tenidap</term>
<term>Therapeutic concentrations</term>
<term>Transcription</term>
<term>Transcription factor</term>
<term>Transcription factors</term>
<term>Transduction</term>
<term>Trends biochem</term>
<term>Tumor necrosis factor</term>
<term>Tyrosine</term>
<term>Tyrosine kinase receptor</term>
<term>Tyrosine kinases</term>
<term>Tyrosine phosphorylation</term>
<term>Various cell types</term>
<term>Various stimuli</term>
<term>Wijkander</term>
<term>Zymosan</term>
<term>Zymosan particles</term>
</keywords>
</textClass>
<langUsage>
<language ident="en">en</language>
</langUsage>
</profileDesc>
</teiHeader>
<front>
<div type="abstract" xml:lang="en">Abstract: 1. 1. Rheumatoid arthritis (RA) is probably the most common source of treatable disability. A major problem in modern rheumatology is that the mechanism(s) of action of the currently used disease-modifying antirheumatic drugs (DMARDs) remain unclear. Many of these drugs entered rheumatology mainly through clinical intuition and have been used for decades. 2. 2. The former T-cell-centered paradigm of rheumatoid inflammation has given way to a model of inflammation highlighting the macrophage and its proinflammatory cytokines. In particular, tumor necrosis factor α (TNF-α) has gained prominence as a central proinflammatory mediator in RA, and antibodies against TNF-α have been successfully used in patients with RA. 3. 3. This review will summarize the recent advances in determining the mechanisms of action of the currently used DMARDs, with particular emphasis on their effects on the induction of TNF-α and interleukin 1 (IL-1) in mononuclear phagocytes. Although some DMARDs, such as auranofin, antimalarials and tenidap, act as inhibitors of the induction of these cytokines in monocytes or macrophages or both, other drugs, such as methotrexate, D-penicillamine and aurothiomalate, do not seem to affect either TNF-α or IL-1. 4. 4. The drugs' effects on proinflammatory cytokine induction are correlated to those on other macrophage responses.</div>
</front>
</TEI>
<affiliations>
<list></list>
<tree>
<noCountry>
<name sortKey="Bondeson, Jan" sort="Bondeson, Jan" uniqKey="Bondeson J" first="Jan" last="Bondeson">Jan Bondeson</name>
</noCountry>
</tree>
</affiliations>
</record>

Pour manipuler ce document sous Unix (Dilib)

EXPLOR_STEP=$WICRI_ROOT/Sante/explor/ChloroquineV1/Data/Main/Exploration
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 002857 | SxmlIndent | more

Ou

HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 002857 | SxmlIndent | more

Pour mettre un lien sur cette page dans le réseau Wicri

{{Explor lien
   |wiki=    Sante
   |area=    ChloroquineV1
   |flux=    Main
   |étape=   Exploration
   |type=    RBID
   |clé=     ISTEX:A6340C83C30596512B99FDF4B12F6E39C5A55E13
   |texte=   The mechanisms of action of disease-modifying antirheumatic drugs: A review with emphasis on macrophage signal transduction and the induction of proinflammatory cytokines
}}

Wicri

This area was generated with Dilib version V0.6.33.
Data generation: Wed Mar 25 22:43:59 2020. Site generation: Sun Jan 31 12:44:45 2021