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Immunological abnormalities as potential biomarkers in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis

Ekua W Brenu12, Mieke L van Driel12, Don R Staines13, Kevin J Ashton2, Sandra B Ramos2, James Keane2, Nancy G Klimas4 and Sonya M Marshall-Gradisnik12*

Author Affiliations

1 Population Health and Neuroimmunology Unit, Faculty of Health Science and Medicine, Bond University, Robina, Queensland, Australia

2 Faculty of Health Science and Medicine, Bond University, Robina, Queensland, Australia

3 Queensland Health, Gold Coast Public Health Unit, Southport, Gold Coast, Queensland, Australia

4 Miami Veterans Affairs Medical Center, Miami, FL, USA

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Journal of Translational Medicine 2011, 9:81  doi:10.1186/1479-5876-9-81

Published: 28 May 2011

Abstract

Background

Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME) is characterised by severe prolonged fatigue, and decreases in cognition and other physiological functions, resulting in severe loss of quality of life, difficult clinical management and high costs to the health care system. To date there is no proven pathomechanism to satisfactorily explain this disorder. Studies have identified abnormalities in immune function but these data are inconsistent. We investigated the profile of markers of immune function (including novel markers) in CFS/ME patients.

Methods

We included 95 CFS/ME patients and 50 healthy controls. All participants were assessed on natural killer (NK) and CD8+T cell cytotoxic activities, Th1 and Th2 cytokine profile of CD4+T cells, expression of vasoactive intestinal peptide receptor 2 (VPACR2), levels of NK phenotypes (CD56bright and CD56dim) and regulatory T cells expressing FoxP3 transcription factor.

Results

Compared to healthy individuals, CFS/ME patients displayed significant increases in IL-10, IFN-γ, TNF-α, CD4+CD25+ T cells, FoxP3 and VPACR2 expression. Cytotoxic activity of NK and CD8+T cells and NK phenotypes, in particular the CD56bright NK cells were significantly decreased in CFS/ME patients. Additionally granzyme A and granzyme K expression were reduced while expression levels of perforin were significantly increased in the CFS/ME population relative to the control population. These data suggest significant dysregulation of the immune system in CFS/ME patients.

Conclusions

Our study found immunological abnormalities which may serve as biomarkers in CFS/ME patients with potential for an application as a diagnostic tool.