JaimeS
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A Preliminary Comparative Assessment of the Role of CD8+T Cells in Chronic Fatigue Syndrome/ Myalgic Encephalomyelitis and Multiple Sclerosis.
Ekua W Brenu1, Simon Broadley3, Thao Nguyen1,2, Samantha Johnston1,2, Sandra Ramos1, Don Staines1, Sonya Marshall- Gradisnik1,2
1The National Centre for Neuroimmunology and Emerging Diseases, Griffith Health Institute, Griffith University, Gold Coast, Australia.
2School of Medical Science, Griffith University, Gold Coast, Australia.
3School of Medicine, Griffith University, Gold Coast, Australia.
Abstract
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 of CD8+T cells in Multiple Sclerosis (MS) and Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME).
Methods
This preliminary investigation comprised of 23 CFS/ME patients, 11 untreated MS patients and 30 non-fatigued 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 naïve, central memory (CM), effector memory CD45RA- (EM cells) and effector memory CD45RA+ (EMRA) cells.
Results
Surface expression of BTLA, CD127 and CD49/CD29 were increased on subsets of CD8+T cells from MS patients. In the CFS/ME patients CD127 was significantly decreased on all subsets of CD8+T cells in comparison to the non-fatigued controls. PSGL-1 was significantly reduced in the CFS/ME patients in comparison to the non-fatigued 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.
Full article attached; it's via Google Scholar, but I have no idea where the original file was posted. I definitely got it for free, though. Please let me know if posting it in its entirety here is inappropriate!
-J
Ekua W Brenu1, Simon Broadley3, Thao Nguyen1,2, Samantha Johnston1,2, Sandra Ramos1, Don Staines1, Sonya Marshall- Gradisnik1,2
1The National Centre for Neuroimmunology and Emerging Diseases, Griffith Health Institute, Griffith University, Gold Coast, Australia.
2School of Medical Science, Griffith University, Gold Coast, Australia.
3School of Medicine, Griffith University, Gold Coast, Australia.
Abstract
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 of CD8+T cells in Multiple Sclerosis (MS) and Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME).
Methods
This preliminary investigation comprised of 23 CFS/ME patients, 11 untreated MS patients and 30 non-fatigued 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 naïve, central memory (CM), effector memory CD45RA- (EM cells) and effector memory CD45RA+ (EMRA) cells.
Results
Surface expression of BTLA, CD127 and CD49/CD29 were increased on subsets of CD8+T cells from MS patients. In the CFS/ME patients CD127 was significantly decreased on all subsets of CD8+T cells in comparison to the non-fatigued controls. PSGL-1 was significantly reduced in the CFS/ME patients in comparison to the non-fatigued 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.
Full article attached; it's via Google Scholar, but I have no idea where the original file was posted. I definitely got it for free, though. Please let me know if posting it in its entirety here is inappropriate!
-J