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Pilot Study of Natural Killer Cells in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis and MS

Kyla

ᴀɴɴɪᴇ ɢꜱᴀᴍᴩᴇʟ
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http://onlinelibrary.wiley.com/doi/10.1111/sji.12388/abstract


Pilot Study of Natural Killer Cells in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis and Multiple Sclerosis.
Huth TK, et al. Scand J Immunol. 2015.

Authors
Huth TK1,2, Brenu EW1,2, Ramos S1,2, Nguyen T1,2, Broadley S3,4, Staines D1,2, Marshall-Gradisnik S1,2.
Author information
  • 1National Centre for Neuroimmunology and Emerging Diseases, Menzies Health Institute Queensland, Griffith University, Southport, QLD, 4222, Australia.
  • 2School of Medical Science, Griffith University, Southport, QLD, 4222, Australia.
  • 3School of Medicine, Griffith University, Southport, QLD, 4222, Australia.
  • 4Gold Coast University Hospital, Southport, QLD, 4222, Australia.
Citation
Scand J Immunol. 2015 Sep 18. doi: 10.1111/sji.12388. [Epub ahead of print]

Abstract
Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME) and Multiple Sclerosis (MS) patients suffer from debilitating fatigue which is not alleviated by rest. In addition to the fatigue related symptoms suffered by CFS/ME and MS patients, dysfunction of the immune system and in particular, reduced Natural Killer (NK) cell cytotoxic activity has also been reported in CFS/ME and MS. The purpose of this pilot study was to compare NK cellular mechanisms in CFS/ME and MS patients to investigate potential dysfunctions in the NK cell activity pathway. Flow cytometry protocols assessed CD56(dim) CD16(+) and CD56(bright) CD16(+/-) NK cell expression of adhesion molecules, NK activating and inhibiting receptors, NK cell maturation and lytic proteins. All participants in this study were female and included 14 CFS/ME patients, 9 MS patients and 19 non-fatigued controls. The patient groups and the non-fatigued controls were not taking any immunosuppressive or immune enhancing medications. In the MS cohort, KIR2DL5 was significantly increased on CD56(bright) CD16(+/-) NK cells and expression of CD94 was significantly increased on CD56(dim) CD16(+) NK cells in comparison to the controls. Co-expression of CD57 and perforin was significantly increased on CD56(dim) CD16(+) NK cells from CFS/ME patients compared to the MS and non-fatigued control participants. The results from this pilot study suggest that NK cells from CFS/ME and MS patients may have undergone increased differentiation in response to external stimuli which may affect different mechanisms in the NK cell cytotoxic activity pathway. This article is protected by copyright. All rights reserved.

This article is protected by copyright. All rights reserved.
PMID
26381393 [PubMed - as supplied by publisher]
 

alex3619

Senior Member
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Location
Logan, Queensland, Australia
What I find interesting is the implication, in combination with the Hornig-Lipkin findings, that ME is best thought of as at least a two dimensional spectrum. Severity, and duration. When you study such a group then the chances of finding key biochemistry goes down until you realize that such stratification is necessary.
 

Kyla

ᴀɴɴɪᴇ ɢꜱᴀᴍᴩᴇʟ
Messages
721
Location
Canada
What I find interesting is the implication, in combination with the Hornig-Lipkin findings, that ME is best thought of as at least a two dimensional spectrum. Severity, and duration. When you study such a group then the chances of finding key biochemistry goes down until you realize that such stratification is necessary.

I have only read the abstract of this one as its paywalled.
Did they stratify by duration and/or severity? I know the last one from this group did.
 

alex3619

Senior Member
Messages
13,810
Location
Logan, Queensland, Australia
I have only read the abstract of this one as its paywalled.
Did they stratify by duration and/or severity? I know the last one from this group did.
I have still not read the full study, I have been having a bad week and a half, and its not getting any easier. I hope to post something in due course.

PS They looked at severity.
 
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