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dc.contributor.authorIracheta-Vellve, Arvin
dc.contributor.authorSzabo, Gyongyi
dc.date2022-08-11T08:09:19.000
dc.date.accessioned2022-08-23T16:26:42Z
dc.date.available2022-08-23T16:26:42Z
dc.date.issued2017-11-20
dc.date.submitted2017-12-06
dc.identifier.citationCell Mol Immunol. 2017 Nov 20. pii: cmi2017108. doi: 10.1038/cmi.2017.108. <a href="https://doi.org/10.1038/cmi.2017.108">Link to article on publisher's site</a>
dc.identifier.issn1672-7681 (Linking)
dc.identifier.doi10.1038/cmi.2017.108
dc.identifier.pmid29151582
dc.identifier.urihttp://hdl.handle.net/20.500.14038/36621
dc.description.abstractMuch controversy surrounds the pathogenesis of acetaminophen-induced inflammation. Acetaminophen (APAP) is a well-studied xenobiotic that in high doses results in a deadly, yet preventable, form of liver failure. Although its effects are sudden and often irreversible, its mechanism is far from simple. In fact, at first glance, recent studies seem to refute each other. The field has been grappling with seemingly contradictory results driven mainly by often-generalized assumptions and different experimental systems. As always, the devil—or in this case, liver failure—is in the details. In this paper, Tang and colleagues identified macrophage-derived interleukin (IL)-1α as a mediator of sterile inflammation in a mouse model of APAP hepatotoxicity. IL-1α is an alarmin that unlike IL-1β, is constitutively expressed in many cells as a precursor. IL-1α precursor (pre-IL-1α) is active as a damage-associated molecular pattern (DAMP). After enzymatic cleavage, mature IL-1α can signal a more potent pro-inflammatory message.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=29151582&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttps://doi.org/10.1038/cmi.2017.108
dc.subjectBiochemistry
dc.subjectCell Biology
dc.subjectCellular and Molecular Physiology
dc.subjectImmunopathology
dc.subjectMolecular Biology
dc.titleIL-1alpha in acetaminophen toxicity: a sterile danger signal
dc.typeLetter to the Editor
dc.source.journaltitleCellular and molecular immunology
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/metnet_pubs/139
dc.identifier.contextkey11207792
html.description.abstract<p>Much controversy surrounds the pathogenesis of acetaminophen-induced inflammation. Acetaminophen (APAP) is a well-studied xenobiotic that in high doses results in a deadly, yet preventable, form of liver failure. Although its effects are sudden and often irreversible, its mechanism is far from simple. In fact, at first glance, recent studies seem to refute each other. The field has been grappling with seemingly contradictory results driven mainly by often-generalized assumptions and different experimental systems. As always, the devil—or in this case, liver failure—is in the details. In this paper, Tang and colleagues identified macrophage-derived interleukin (IL)-1α as a mediator of sterile inflammation in a mouse model of APAP hepatotoxicity. IL-1α is an alarmin that unlike IL-1β, is constitutively expressed in many cells as a precursor. IL-1α precursor (pre-IL-1α) is active as a damage-associated molecular pattern (DAMP). After enzymatic cleavage, mature IL-1α can signal a more potent pro-inflammatory message.</p>
dc.identifier.submissionpathmetnet_pubs/139
dc.contributor.departmentUMass Metabolic Network
dc.contributor.departmentDepartment of Medicine, Division of Gastroenterology
dc.contributor.departmentGraduate School of Biomedical Sciences, Translational Science Program


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