| http://purl.uniprot.org/citations/18490713 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/18490713 | http://www.w3.org/2000/01/rdf-schema#comment | "The proinflammatory IL-1 cytokines IL-1alpha, IL-1beta, and IL-18 are key mediators of the acute immune response to injury and infection. Mechanisms underlying their cellular release remain unclear. Activation of purinergic P2X(7) receptors (P2X(7)R) by extracellular ATP is a key physiological inducer of rapid IL-1beta release from LPS-primed macrophage. We investigated patterns of ATP-mediated release of IL-1 cytokines from three macrophage types in attempts to provide direct evidence for or against distinct release mechanisms. We used peritoneal macrophage from P2X(7)R(-/-) mice and found that release of IL-1alpha, IL-18, as well as IL-1beta, by ATP resulted exclusively from activation of P2X(7)R, release of all these IL-1 cytokines involved pannexin-1 (panx1), and that there was both a panx1-dependent and -independent component to IL-1beta release. We compared IL-1-release patterns from LPS-primed peritoneal macrophage, RAW264.7 macrophage, and J774A.1 macrophage. We found RAW264.7 macrophage readily release pro-IL-1beta independently of panx1 but do not release mature IL-1beta because they do not express apoptotic speck-like protein with a caspase-activating recruiting domain and so have no caspase-1 inflammasome activity. We delineated two distinct release pathways: the well-known caspase-1 cascade mediating release of processed IL-1beta that was selectively blocked by inhibition of caspase-1 or panx1, and a calcium-independent, caspase-1/panx1-independent release of pro-IL-1beta that was selectively blocked by glycine. None of these release responses were associated with cell damage or cytolytic effects. This provides the first direct demonstration of a distinct signaling mechanism responsible for ATP-induced release of pro-IL-1beta."xsd:string |
| http://purl.uniprot.org/citations/18490713 | http://purl.org/dc/terms/identifier | "doi:10.4049/jimmunol.180.11.7147"xsd:string |
| http://purl.uniprot.org/citations/18490713 | http://purl.uniprot.org/core/author | "Pelegrin P."xsd:string |
| http://purl.uniprot.org/citations/18490713 | http://purl.uniprot.org/core/author | "Surprenant A."xsd:string |
| http://purl.uniprot.org/citations/18490713 | http://purl.uniprot.org/core/author | "Barroso-Gutierrez C."xsd:string |
| http://purl.uniprot.org/citations/18490713 | http://purl.uniprot.org/core/date | "2008"xsd:gYear |
| http://purl.uniprot.org/citations/18490713 | http://purl.uniprot.org/core/name | "J Immunol"xsd:string |
| http://purl.uniprot.org/citations/18490713 | http://purl.uniprot.org/core/pages | "7147-7157"xsd:string |
| http://purl.uniprot.org/citations/18490713 | http://purl.uniprot.org/core/title | "P2X7 receptor differentially couples to distinct release pathways for IL-1beta in mouse macrophage."xsd:string |
| http://purl.uniprot.org/citations/18490713 | http://purl.uniprot.org/core/volume | "180"xsd:string |
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