alexa Characterization of Natural Killer Cell Phenotypes in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis | OMICS International | Abstract
ISSN: 2155-9899

Journal of Clinical & Cellular Immunology
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Research Article

Characterization of Natural Killer Cell Phenotypes in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis

Teilah K. Huth1,2*, Ekua W. Brenu1,2, Thao Nguyen1,2, Sharni L. Hardcastle1,2, Samantha Johnston1,2, Sandra Ramos1,2, Donald R. Staines2,3 and Sonya M. Marshall-Gradisnik1,2
1National Centre for Neuroimmunology and Emerging Diseases, Griffith Health Institute, Griffith University, Southport, QLD, Australia
2School of Medical Science, Griffith University, Southport, QLD, Australia
3Queensland Health, Gold Coast Public Health Unit, Robina, QLD, Australia
Corresponding Author : Teilah Huth
BBioMedSc(Hons)
National Centre for Neuroimmunology and Emerging Diseases
Griffith Health Institute, Griffith University
Parklands, QLD 4222, Australia
Tel: +61 7 5678 9283
E-mail: [email protected]
Received: April 22, 2014; Accepted: June 07, 2014; Published: June 14, 2014
Citation: Huth TK, Brenu EW, Nguyen T, Hardcastle SL, Johnston S, et al. (2014) Characterization of Natural Killer Cell Phenotypes in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis . J Clin Cell Immunol 5:223. doi:10.4172/2155-9899.1000223
Copyright: © 2014 Huth TK, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Abstract

Objective: Natural Killer (NK) cells are classified into different phenotypes according to the expression of the surface markers CD56 and CD16. Each NK cell phenotype has a role in the immune response through cytotoxic activity or cytokine production. Reduced NK cell cytotoxic activity is a consistent finding in patients with Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME) and investigations into the potential causes of reduced NK cell cytotoxic activity have predominantly focused on total NK cells. The purpose of this study was to investigate and characterize four NK cell phenotypes in CFS/ME.

Methods: Twenty nine CFS/ME patients (mean age ± SEM=48.28 ± 2.63) meeting the 1994 Fukuda definition and 27 healthy controls (mean age ± SEM=49.15 ± 2.51) were included in this study. Flow cytometric protocols identified CD56brightCD16-/dim, CD56dimCD16-, CD56dimCD16+ or CD56-CD16+ NK cells for the measurement of surface markers including adhesion molecules CD2, CD18, CD11a, CD11b and CD11c, natural cytotoxicity receptors, Killer Immunoglobulin Like Receptors, signalling lymphocytic activation molecules and cell maturation (CD57). Following stimulation, NK cell phenotype expression of CD107a and CD107b was measured as a marker for degranulation. Intracellular staining measured lytic proteins including perforin, Granzyme A and Granzyme B in the four NK cell phenotypes.

Results: In the CFS/ME group, CD56brightCD16-/dim NK cell co-expression of adhesion molecules CD2 and CD18 was significantly reduced. Granzyme B was significantly decreased in CD56dimCD16+ and CD56-CD16+ NK cells from CFS/ME patients. CD57 expression on CD56dimCD16+ NK cells from CFS/ME patients was significantly increased.

Conclusion: This is the first study to characterize four NK cell phenotypes in CFS/ME by investigating surface and intracellular molecules necessary for NK cell effector function. The data suggests that a combination of impairments in CD56dimCD16+ NK cells from CFS/ME patients may contribute to reduced cytotoxic activity of this phenotype.

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