Linked Life Data

17692395

Source:http://linkedlifedata.com/resource/pubmed/id/17692395

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2007-9-11
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.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0165-6147
pubmed:author
pubmed:issnType
Print
pubmed:volume
28
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
465-72
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Liaisons dangereuses: P2X(7) and the inflammasome.
pubmed:affiliation
Department of Experimental and Diagnostic Medicine, Section of General Pathology, University of Ferrara, Via Borsari, 46, Ferrara, Italy. fdv@unife.it
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't