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dc.contributor.authorNguyen, T
dc.contributor.authorJohnston, S
dc.contributor.authorClarke, L
dc.contributor.authorSmith, P
dc.contributor.authorStaines, D
dc.contributor.authorMarshall-Gradisnik, S
dc.date.accessioned2019-01-30T12:30:52Z
dc.date.available2019-01-30T12:30:52Z
dc.date.issued2017
dc.identifier.issn0009-9104
dc.identifier.doi10.1111/cei.12882
dc.identifier.urihttp://hdl.handle.net/10072/124048
dc.description.abstractTransient receptor potential melastatin subfamily 3 (TRPM3) ion channels play a role in calcium (Ca2+) cell signalling. Reduced TRPM3 protein expression has been identified in chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) patients. However, the significance of TRPM3 and association with intracellular Ca2+ mobilization has yet to be determined. Fifteen CFS/ME patients (mean age 48·82 ± 9·83 years) and 25 healthy controls (mean age 39·2 ± 12·12 years) were examined. Isolated natural killer (NK) cells were labelled with fluorescent antibodies to determine TRPM3, CD107a and CD69 receptors on CD56dimCD16+NK cells and CD56brightCD16dim/– NK cells. Ca2+ flux and NK cytotoxicity activity was measured under various stimulants, including pregnenolone sulphate (PregS), thapsigargin (TG), 2‐aminoethoxydiphenyl borate (2APB) and ionomycin. Unstimulated CD56brightCD16dim/– NK cells showed significantly reduced TRPM3 receptors in CFS/ME compared with healthy controls (HC). Ca2+ flux showed no significant difference between groups. Moreover, PregS‐stimulated CD56brightCD16dim/–NK cells showed a significant increase in Ca2+ flux in CFS/ME patients compared with HC. By comparison, unstimulated CD56dimCD16+ NK cells showed no significant difference in both Ca2+ flux and TRPM3 expression. PregS‐stimulated CD56dimCD16+ NK cells increased TRPM3 expression significantly in CFS/ME, but this was not associated with a significant increase in Ca2+ flux. Furthermore, TG‐stimulated CD56dimCD16+ NK cells increased K562 cell lysis prior to PregS stimulation in CFS/ME patients compared with HC. Differential expression of TRPM3 and Ca2+ flux between NK cell subtypes may provide evidence for their role in the pathomechanism involving NK cell cytotoxicity activity in CFS/ME.
dc.description.peerreviewedYes
dc.languageEnglish
dc.language.isoeng
dc.publisherWiley-Blackwell Publishing
dc.relation.ispartofpagefrom284
dc.relation.ispartofpageto293
dc.relation.ispartofissue2
dc.relation.ispartofjournalClinical and Experimental Immunology
dc.relation.ispartofvolume187
dc.subject.fieldofresearchCellular Immunology
dc.subject.fieldofresearchImmunology not elsewhere classified
dc.subject.fieldofresearchMedical and Health Sciences not elsewhere classified
dc.subject.fieldofresearchImmunology
dc.subject.fieldofresearchcode110704
dc.subject.fieldofresearchcode110799
dc.subject.fieldofresearchcode119999
dc.subject.fieldofresearchcode1107
dc.titleImpaired calcium mobilization in natural killer cells from chronic fatigue syndrome/myalgic encephalomyelitis patients is associated with transient receptor potential melastatin 3 ion channels
dc.typeJournal article
dc.type.descriptionC1 - Articles
dc.type.codeC - Journal Articles
dcterms.licensehttp://creativecommons.org/licenses/by-nc/4.0/
dc.description.versionVersion of Record (VoR)
gro.facultyGriffith Health, School of Medical Science
gro.description.notepublicThis publication has been entered into Griffith Research Online as an Advanced Online Version.
gro.rights.copyright© 2016 The Authors. Clinical & Experimental Immunology published by John Wiley & Sons Ltd on behalf of British Society for Immunology, Clinical and Experimental Immunology, 187: 284–293. This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.
gro.hasfulltextFull Text
gro.griffith.authorStaines, Donald R.
gro.griffith.authorSmith, Peter K.
gro.griffith.authorMarshall-Gradisnik, Sonya M.
gro.griffith.authorJohnston, Samantha
gro.griffith.authorNguyen, Thao
gro.griffith.authorClarke, Laura


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