Source:http://linkedlifedata.com/resource/pubmed/id/18782014
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2008-9-10
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pubmed:abstractText |
Maintaining health requires a dynamic balance between the influence of pro-inflammatory and anti-inflammatory mediators. While inflammation serves an important protective role against infection, unrestrained inflammation is acutely lethal and unresolved inflammation contributes to a broad range of chronic disorders. Immunotherapy with cytokines themselves or cytokine antagonists faces strict limitations due to efficacy, safety and cost. More successful treatment of the pro-inflammatory component of chronic disorders may emerge from strategies designed to reset the balance between pro and anti-inflammatory cytokines through physiological regulatory pathways. One emerging avenue for this approach is exploitation of the link between the cell surface protein CD36 and the anti-inflammatory cytokine interleukin-10 (IL-10). Agents that increase CD36 expression and agents that directly bind to CD36 have anti-inflammatory properties that may directly relate to induction of IL-10. The immunosuppressive effects of apoptotic cells were first reported more than a decade ago and have since been tested in animal models and several clinical trials. A recent publication demonstrates that induction of IL-10 by apoptotic cells is largely dependent upon the interaction between apoptotic cells and CD36, the receptor on monocytes and macrophages for apoptotic cells. This provides a direct mechanistic link between CD36 engagement and IL-10 induction, opening up new possibilities for using CD36 ligands, agents that increase CD36 expression or a combination of both to modulate inflammation and treat, or even prevent, an important set of chronic disorders.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
1871-5303
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
8
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
184-91
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pubmed:meshHeading |
pubmed-meshheading:18782014-Animals,
pubmed-meshheading:18782014-Anti-Inflammatory Agents,
pubmed-meshheading:18782014-Antigens, CD36,
pubmed-meshheading:18782014-Apoptosis,
pubmed-meshheading:18782014-Humans,
pubmed-meshheading:18782014-Inflammation,
pubmed-meshheading:18782014-Interleukin-10,
pubmed-meshheading:18782014-PPAR gamma
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pubmed:year |
2008
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pubmed:articleTitle |
Harnessing CD36 to rein in inflammation.
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pubmed:affiliation |
Immunology Program, Division of basic Medical Sciences, Faculty of Medicine, Memorial University of Newfoundland, 300 Prince Philip Drive, St. John's, NL, Canada A1B 3V6.
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pubmed:publicationType |
Journal Article,
Review,
Research Support, Non-U.S. Gov't
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