Show simple item record

dc.contributor.authorCarpenter, Susan
dc.contributor.authorCarlson, Thaddeus
dc.contributor.authorDellacasagrande, Jerome
dc.contributor.authorGarcia, Amaya
dc.contributor.authorGibbons, Sharon
dc.contributor.authorHertzog, Paul
dc.contributor.authorLyons, Anthony
dc.contributor.authorLin, Lih-Ling
dc.contributor.authorLynch, Marina
dc.contributor.authorMonie, Tom
dc.contributor.authorMurphy, Caroline
dc.contributor.authorSeidl, Katherine J
dc.contributor.authorWells, Christine
dc.contributor.authorDunne, Aisling
dc.contributor.authorO'Neill, Luke AJ
dc.date.accessioned2017-05-03T15:01:02Z
dc.date.available2017-05-03T15:01:02Z
dc.date.issued2009
dc.date.modified2010-06-18T03:56:16Z
dc.identifier.issn0022-1767
dc.identifier.doi10.4049/jimmunol.0901518
dc.identifier.urihttp://hdl.handle.net/10072/30545
dc.description.abstractTLR4 is the primary sensor of LPS. In this study, we describe for the first time TLR4 interactor with leucine-rich repeats (TRIL), which is a novel component of the TLR4 complex. TRIL is expressed in a number of tissues, most prominently in the brain but also in the spinal cord, lung, kidney, and ovary. TRIL is composed of a signal sequence, 13 leucine-rich repeats, a fibronectin domain, and a single transmembrane spanning region. TRIL is induced by LPS in the human astrocytoma cell line U373, in murine brain following i.p. injection, and in human PBMC. Endogenous TRIL interacts with TLR4 and this interaction is greatly enhanced following LPS stimulation. TRIL also interacts with the TLR4 ligand LPS. Furthermore, U373 cells stably overexpressing TRIL display enhanced cytokine production in response to LPS. Finally, knockdown of TRIL using small interfering RNA attenuates LPS signaling and cytokine production in cell lines, human PBMC, and primary murine mixed glial cells. These results demonstrate that TRIL is a novel component of the TLR4 complex which may have particular relevance for the functional role of TLR4 in the brain.
dc.description.peerreviewedYes
dc.description.publicationstatusYes
dc.languageEnglish
dc.language.isoeng
dc.publisherThe American Association of Immunologists, Inc.
dc.publisher.placeUSA
dc.relation.ispartofstudentpublicationN
dc.relation.ispartofpagefrom3989
dc.relation.ispartofpageto3995
dc.relation.ispartofjournalJournal of Immunology
dc.relation.ispartofvolume183
dc.rights.retentionY
dc.subject.fieldofresearchOther biological sciences not elsewhere classified
dc.subject.fieldofresearchImmunology
dc.subject.fieldofresearchcode319999
dc.subject.fieldofresearchcode3204
dc.titleTRIL, a Functional Component of the TLR4 Signaling Complex, Highly Expressed in Brain
dc.typeJournal article
dc.type.descriptionC1 - Articles
dc.type.codeC - Journal Articles
gro.rights.copyright© 2009 AAI. Self-archiving of the author-manuscript version is not yet supported by this publisher. Please refer to the journal link for access to the definitive, published version or contact the authors for more information.
gro.date.issued2009
gro.hasfulltextNo Full Text
gro.griffith.authorWells, Christine


Files in this item

FilesSizeFormatView

There are no files associated with this item.

This item appears in the following Collection(s)

  • Journal articles
    Contains articles published by Griffith authors in scholarly journals.

Show simple item record