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- aggregation classification "A1".
- aggregation creator B356098.
- aggregation creator person.
- aggregation creator person.
- aggregation creator person.
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- aggregation creator person.
- aggregation creator person.
- aggregation date "2012".
- aggregation format "application/pdf".
- aggregation hasFormat 2095247.bibtex.
- aggregation hasFormat 2095247.csv.
- aggregation hasFormat 2095247.dc.
- aggregation hasFormat 2095247.didl.
- aggregation hasFormat 2095247.doc.
- aggregation hasFormat 2095247.json.
- aggregation hasFormat 2095247.mets.
- aggregation hasFormat 2095247.mods.
- aggregation hasFormat 2095247.rdf.
- aggregation hasFormat 2095247.ris.
- aggregation hasFormat 2095247.txt.
- aggregation hasFormat 2095247.xls.
- aggregation hasFormat 2095247.yaml.
- aggregation isPartOf urn:issn:1553-7366.
- aggregation language "eng".
- aggregation rights "I have retained and own the full copyright for this publication".
- aggregation subject "Biology and Life Sciences".
- aggregation title "A20 (Tnfaip3) deficiency in myeloid cells protects against influenza A virus infection".
- aggregation abstract "The innate immune response provides the first line of defense against viruses and other pathogens by responding to specific microbial molecules. Influenza A virus (IAV) produces double-stranded RNA as an intermediate during the replication life cycle, which activates the intracellular pathogen recognition receptor RIG-I and induces the production of proinflammatory cytokines and antiviral interferon. Understanding the mechanisms that regulate innate immune responses to IAV and other viruses is of key importance to develop novel therapeutic strategies. Here we used myeloid cell specific A20 knockout mice to examine the role of the ubiquitin-editing protein A20 in the response of myeloid cells to IAV infection. A20 deficient macrophages were hyperresponsive to double stranded RNA and IAV infection, as illustrated by enhanced NF-kappa B and IRF3 activation, concomitant with increased production of proinflammatory cytokines, chemokines and type I interferon. In vivo this was associated with an increased number of alveolar macrophages and neutrophils in the lungs of IAV infected mice. Surprisingly, myeloid cell specific A20 knockout mice are protected against lethal IAV infection. These results challenge the general belief that an excessive host proinflammatory response is associated with IAV-induced lethality, and suggest that under certain conditions inhibition of A20 might be of interest in the management of IAV infections.".
- aggregation authorList BK656699.
- aggregation issue "3".
- aggregation volume "8".
- aggregation aggregates 4381242.
- aggregation isDescribedBy 2095247.
- aggregation similarTo journal.ppat.1002570.
- aggregation similarTo LU-2095247.