| pubmed-article:17692395 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17692395 | lifeskim:mentions | umls-concept:C0683597 | lld:lifeskim |
| pubmed-article:17692395 | pubmed:issue | 9 | lld:pubmed |
| pubmed-article:17692395 | pubmed:dateCreated | 2007-9-11 | lld:pubmed |
| pubmed-article:17692395 | pubmed:abstractText | Inflammation is initiated by specific pathogen constituents, in addition to intrinsic host molecules that are released by injured or dying cells. Among such host endogenous pro-inflammatory factors, nucleotides (mainly ATP) are attracting increasing interest for their potential as natural adjuvants. Extracellular ATP stimulates a family of receptors, named P2, one of which, P2X(7), is a potent mediator of interleukin (IL)-1beta and IL-18 processing and release. The mechanism and physiological significance of this unusual pro-inflammatory activity have long remained elusive. Recent data unveiling the structure and function of a novel caspase-activating platform, the inflammasome, shed light on P2X(7) receptor coupling to IL-1beta release, and suggest a fascinating scenario for the initiation and amplification of the innate immune response. Here, I outline the intriguing links between the P2X(7) receptor and the NALP3 inflammasome, review recent evidence showing that this receptor is a potent activator of this multimolecular platform and discuss implications for pathogen-immune cell interaction and for anti-inflammatory drug development. | lld:pubmed |
| pubmed-article:17692395 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17692395 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17692395 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:17692395 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17692395 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:17692395 | pubmed:issn | 0165-6147 | lld:pubmed |
| pubmed-article:17692395 | pubmed:author | pubmed-author:Di... | lld:pubmed |
| pubmed-article:17692395 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17692395 | pubmed:volume | 28 | lld:pubmed |
| pubmed-article:17692395 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17692395 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17692395 | pubmed:pagination | 465-72 | lld:pubmed |
| pubmed-article:17692395 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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| pubmed-article:17692395 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:17692395 | pubmed:articleTitle | Liaisons dangereuses: P2X(7) and the inflammasome. | lld:pubmed |
| pubmed-article:17692395 | pubmed:affiliation | Department of Experimental and Diagnostic Medicine, Section of General Pathology, University of Ferrara, Via Borsari, 46, Ferrara, Italy. fdv@unife.it | lld:pubmed |
| pubmed-article:17692395 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:17692395 | pubmed:publicationType | Review | lld:pubmed |
| pubmed-article:17692395 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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