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dc.contributor.authorSzvetko, Attila
dc.contributor.authorJones, Ashleigh
dc.contributor.authorMackenzie, Jason
dc.contributor.authorTajouri, Lotfi
dc.contributor.authorCsurhes, Peter A.
dc.contributor.authorGreer, Judith M.
dc.contributor.authorPender, Michael P.
dc.contributor.authorGriffiths, Lyn
dc.date.accessioned2017-05-03T14:36:40Z
dc.date.available2017-05-03T14:36:40Z
dc.date.issued2010
dc.date.modified2011-06-16T06:03:34Z
dc.identifier.issn01616412
dc.identifier.doi10.1179/174313209X405155
dc.identifier.urihttp://hdl.handle.net/10072/30522
dc.description.abstractMultiple sclerosis (MS) is a serious cause of neurological disability among young adults. The clinical course remains difficult to predict, and the pathogenesis of the disease is still modestly understood. Autoimmunity is thought to be a key aspect of the disease, with autoreactive T cells thought to mediate central nervous system (CNS) inflammation to some extent. Toll-like receptors are known to mediate cellular recognition of pathogens by way of patterns of molecular presentation. Toll-like receptor 3 is coded by the gene TLR3 and is recognized as an important factor in virus recognition and is known to be involved in the expression of neuroprotective mediators. We set out to investigate two variations within the TLR3 gene, an 8 bp insertion-deletion [ -/A]8 and a single base-pair variation C1236T, in subjects with MS and matched healthy controls to determine whether significant differences exist in these markers in an Australian population. We used capillary gel electrophoresis and TaqMan genotyping assay techniques to resolve genotypes for each marker, respectively. Our work found no significant difference between frequencies for TLR3 [ -/A]8 by genotype (x2=1.03, p=0.60) or allele (x2=1.09, p=0.30). Similarly, we found no evidence for the association of TLR3 C1236T by genotype (x2=0.35, p=0.84) or allele frequency (x2=0.31, p=0.58). This work reveals no evidence to suggest that these markers are associated with MS in the tested population. Although the role of TLR3 and the wider toll-like receptor family remain significant in neurological and CNS inflammatory disorders, our current work does not support a role for the two tested variants in this gene with regard to MS susceptibility.
dc.description.peerreviewedYes
dc.description.publicationstatusYes
dc.format.extent82374 bytes
dc.format.mimetypeapplication/pdf
dc.languageEnglish
dc.language.isoeng
dc.publisherManey Publishing
dc.publisher.placeUnited Kingdom
dc.relation.ispartofstudentpublicationY
dc.relation.ispartofpagefrom438
dc.relation.ispartofpageto441
dc.relation.ispartofissue4
dc.relation.ispartofjournalNeurological Research
dc.relation.ispartofvolume32
dc.rights.retentionY
dc.subject.fieldofresearchNeurogenetics
dc.subject.fieldofresearchClinical sciences
dc.subject.fieldofresearchNeurosciences
dc.subject.fieldofresearchcode310511
dc.subject.fieldofresearchcode3202
dc.subject.fieldofresearchcode3209
dc.titleInvestigation of the [-/A]8 and C1236T genetic variations within the human toll-like receptor 3 gene for the association with multiple sclerosis
dc.typeJournal article
dc.type.descriptionC1 - Articles
dc.type.codeC - Journal Articles
gro.facultyGriffith Health, School of Medical Science
gro.rights.copyright© 2009 Maney Publishing. The attached file is reproduced here in accordance with the copyright policy of the publisher. Please refer to the journal's website for access to the definitive, published version.
gro.date.issued2010
gro.hasfulltextFull Text
gro.griffith.authorTajouri, Lotfi
gro.griffith.authorGriffiths, Lyn
gro.griffith.authorSzvetko, Attila L.
gro.griffith.authorMackenzie, Jason
gro.griffith.authorJones, Ashleigh R.


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