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dc.contributor.authorClarke, Lauraen_US
dc.contributor.authorBroadley, Simonen_US
dc.contributor.authorNguyen, Thaoen_US
dc.contributor.authorJohnston, Samanthaen_US
dc.contributor.authorEaton, Natalieen_US
dc.contributor.authorStaines, Donalden_US
dc.contributor.authorMarshall-Gradisnik, Sonyaen_US
dc.date.accessioned2019-05-29T12:41:56Z
dc.date.available2019-05-29T12:41:56Z
dc.date.issued2018en_US
dc.identifier.issn2158-284Xen_US
dc.identifier.doi10.4236/ijcm.2018.97047en_US
dc.identifier.urihttp://hdl.handle.net/10072/382204
dc.description.abstractBackground: Natural killer (NK) cell phenotypes have reported to be implicated in the pathomechanism of Multiple Sclerosis (MS). Several investigators have observed reduced peripheral numbers, reduced cytotoxic activity, and altered CD56Dim and CD56Bright NK cell phenotypes. This current project, for the first time, investigates the NK cell cytotoxicity, calcium mobilisation and transient receptor potential melastatin 3 (TRPM3) surface expression. Methods: NK cell cytotoxic activity and calcium signaling were examined in CD56Dim and CD56Bright NK cells before and after stimulation using Ionomycin, Pregnenolone sulphate, 2-Aminoethoxydiphenyl borate and Thapsigargin. Purified NK cells were labelled with antibodies to determine TRPM3, CD69 and CD107a surface expression using flow cytometry. Results: Twenty-two MS patients and 22 healthy controls were recruited for this project. Twelve of the 22 previously received Alemtuzumab (LemtradaÒ) and the remaining ten reported nil medication. We report TRPM3 was significantly increased in untreated MS patients compared with healthy controls and treated MS patients (p-value 0.034). There was a significant decrease in CD69 surface expression on CD56Dim NK cell phenotype for untreated MS patients (p-value 0.031) and treated MS patients (p-value 0.036). We report altered calcium mobilisation in CD56Bright NK cells and to a lesser extent CD56Dim NK cells between healthy controls, treated and untreated MS patients. Conclusion: This investigation suggests variations in TRPM3 expression and calcium mobilisation of NK cells may be implicated in the pathogenesis of MS. Further investigation is required to determine the mechanism by which alemtuzumab alters calcium signaling in NK cells.en_US
dc.description.peerreviewedYesen_US
dc.languageEnglishen_US
dc.publisherScientific Research Publishingen_US
dc.publisher.placeUnited Statesen_US
dc.relation.ispartofpagefrom541en_US
dc.relation.ispartofpageto565en_US
dc.relation.ispartofissue7en_US
dc.relation.ispartofjournalInternational Journal of Clinical Medicineen_US
dc.relation.ispartofvolume9en_US
dc.subject.fieldofresearchCellular Immunologyen_US
dc.subject.fieldofresearchImmunology not elsewhere classifieden_US
dc.subject.fieldofresearchMedical and Health Sciences not elsewhere classifieden_US
dc.subject.fieldofresearchcode110704en_US
dc.subject.fieldofresearchcode110799en_US
dc.subject.fieldofresearchcode119999en_US
dc.titleTransient Receptor Potential Melastatin 3 and Intracellular Calcium in Natural Killer Cells in Multiple Sclerosisen_US
dc.typeJournal articleen_US
dc.type.descriptionC1 - Articlesen_US
dc.type.codeC - Journal Articlesen_US
dcterms.licensehttp://creativecommons.org/licenses/by/3.0/en_US
dc.description.versionPublisheden_US
gro.facultyGriffith Health, School of Medical Scienceen_US
gro.rights.copyright© 2018 The author(s) and SciRes. This is an Open Access article distributed under the terms of the Creative Commons Attribution 3.0 Unported (CC BY 3.0) License (http://creativecommons.org/licenses/by/3.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.en_US
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