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dc.contributor.authorFALLON, PADRAICen
dc.date.accessioned2015-01-14T14:24:42Z
dc.date.available2015-01-14T14:24:42Z
dc.date.issued2013en
dc.date.submitted2013en
dc.identifier.citationScalfone LK, Nel HJ, Gagliardo LF, Cameron JL, Al-Shokri S, Leifer CA, Fallon PG, Appleton JA., Participation of MyD88 and interleukin-33 as innate drivers of Th2 immunity to Trichinella spiralis., Infect Immun, 81, 2013, 1354 - 1363en
dc.identifier.otherYen
dc.identifier.urihttp://hdl.handle.net/2262/72993
dc.descriptionPUBLISHEDen
dc.description.abstractTrichinella spiralis is a highly destructive parasitic nematode that invades and destroys intestinal epithelial cells, injures many different tissues during its migratory phase, and occupies and transforms myotubes during the final phase of its life cycle. We set out to investigate the role in immunity of innate receptors for potential pathogen- or danger-associated molecular patterns (PAMPs or DAMPs). Focusing on the MyD88-dependent receptors, which include Toll-like receptors (TLRs) and interleukin-1 (IL-1) family members, we found that MyD88-deficient mice expelled worms normally, while TLR2/4-deficient mice showed accelerated worm expulsion, suggesting that MyD88 was active in signaling pathways for more than one receptor during intestinal immunity. A direct role for PAMPs in TLR activation was not supported in a transactivation assay involving a panel of murine and human TLRs. Mice deficient in the IL-1 family receptor for the DAMP, IL-33 (called ST2), displayed reduced intestinal Th2 responses and impaired mast cell activation. IL-33 was constitutively expressed in intestinal epithelial cells, where it became concentrated in nuclei within 2 days of infection. Nuclear localization was an innate response to infection that occurred in intestinal regions where worms were actively migrating. Th2 responses were also compromised in the lymph nodes draining the skeletal muscles of ST2-deficient mice, and this correlated with increased larval burdens in muscle. Our results support a mechanism in which the immune system recognizes and responds to tissue injury in a way that promotes Th2 responses.en
dc.format.extent1354en
dc.format.extent1363en
dc.language.isoenen
dc.relation.ispartofseriesInfect Immunen
dc.relation.ispartofseries81en
dc.rightsYen
dc.subjectToll-like receptorsen
dc.titleParticipation of MyD88 and interleukin-33 as innate drivers of Th2 immunity to Trichinella spiralis.en
dc.typeJournal Articleen
dc.contributor.sponsorScience Foundation Ireland (SFI)en
dc.type.supercollectionscholarly_publicationsen
dc.type.supercollectionrefereed_publicationsen
dc.identifier.peoplefinderurlhttp://people.tcd.ie/pfallonen
dc.identifier.rssinternalid96754en
dc.identifier.doihttp://dx.doi.org/10.1128/IAI.01307-12en
dc.rights.ecaccessrightsopenAccess
dc.subject.TCDThemeImmunology, Inflammation & Infectionen
dc.subject.TCDTagBiomedical sciencesen


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