A Preliminary Comparative Assessment of the Role of CD8+ T Cells in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis and Multiple Sclerosis

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Author(s)
Brenu, Ekua W
Broadley, Simon
Thao, Nguyen
Johnston, Samantha
Ramos, Sandra
Staines, Don
Marshall-Gradisnik, Sonya
Griffith University Author(s)
Year published
2016
Metadata
Show full item recordAbstract
Background. CD8+ T cells have putative roles in the regulation of adaptive immune responses during infection.The purpose of this
paper is to compare the status ofCD8+ T cells inMultiple Sclerosis (MS) andChronic Fatigue Syndrome/Myalgic Encephalomyelitis
(CFS/ME). Methods.This preliminary investigation comprised 23 CFS/ME patients, 11 untreated MS patients, and 30 nonfatigued
controls. Whole blood samples were collected from participants, stained with monoclonal antibodies, and analysed on the flow
cytometer. Using the following CD markers, CD27 and CD45RA (CD45 exon isoform 4), CD8+ T cells were divided into
na¨ıve, central ...
View more >Background. CD8+ T cells have putative roles in the regulation of adaptive immune responses during infection.The purpose of this paper is to compare the status ofCD8+ T cells inMultiple Sclerosis (MS) andChronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME). Methods.This preliminary investigation comprised 23 CFS/ME patients, 11 untreated MS patients, and 30 nonfatigued controls. Whole blood samples were collected from participants, stained with monoclonal antibodies, and analysed on the flow cytometer. Using the following CD markers, CD27 and CD45RA (CD45 exon isoform 4), CD8+ T cells were divided into na¨ıve, central memory (CM), effector memory CD45RA− (EM), and effector memory CD45RA+ (EMRA) cells. Results. Surface expressions of BTLA, CD127, and CD49/CD29 were increased on subsets of CD8+ T cells fromMS patients. In the CFS/ME patients CD127was significantly decreased on all subsets ofCD8+Tcells in comparison to the nonfatigued controls. PSGL-1was significantly reduced in the CFS/ME patients in comparison to the nonfatigued controls. Conclusions.The results suggest significant deficits in the expression of receptors and adhesion molecules on subsets of CD8+ T cells in both MS and CFS/ME patients. These deficits reported may contribute to the pathogenesis of these diseases. However, larger sample size is warranted to confirm and support these encouraging preliminary findings.
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View more >Background. CD8+ T cells have putative roles in the regulation of adaptive immune responses during infection.The purpose of this paper is to compare the status ofCD8+ T cells inMultiple Sclerosis (MS) andChronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME). Methods.This preliminary investigation comprised 23 CFS/ME patients, 11 untreated MS patients, and 30 nonfatigued controls. Whole blood samples were collected from participants, stained with monoclonal antibodies, and analysed on the flow cytometer. Using the following CD markers, CD27 and CD45RA (CD45 exon isoform 4), CD8+ T cells were divided into na¨ıve, central memory (CM), effector memory CD45RA− (EM), and effector memory CD45RA+ (EMRA) cells. Results. Surface expressions of BTLA, CD127, and CD49/CD29 were increased on subsets of CD8+ T cells fromMS patients. In the CFS/ME patients CD127was significantly decreased on all subsets ofCD8+Tcells in comparison to the nonfatigued controls. PSGL-1was significantly reduced in the CFS/ME patients in comparison to the nonfatigued controls. Conclusions.The results suggest significant deficits in the expression of receptors and adhesion molecules on subsets of CD8+ T cells in both MS and CFS/ME patients. These deficits reported may contribute to the pathogenesis of these diseases. However, larger sample size is warranted to confirm and support these encouraging preliminary findings.
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Journal Title
Journal of Immunology Research
Copyright Statement
© 2016 EkuaW. Brenu et al. This is an open access article distributed under the Creative Commons Attribution License,
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Note
This publication has been entered into Griffith Research Online as an Advanced Online Version.
Subject
Immunology not elsewhere classified