Longitudinal investigation of natural killer cells and cytokines in chronic fatigue syndrome/myalgic encephalomyelitis
Open accessAbstract
BACKGROUND: Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME) is an etiologically unexplained disorder characterised by irregularities in various aspects of the immunological function. Presently, it is unknown whether these immunological changes remain consistent over time. This study investigates Natural Killer (NK) cell cytotoxic activity, NK cell subsets (CD56brightCD16- and CD56dimCD16+) and cytokines, over the course of a12 month period in patients with CFS/ME. METHODS: The participants in the study comprised 65 (47.2 ± 11.5 years) CFS/ME participants and 21 (45.2 ± 9.3 years) non-fatigued controls. Flow cytometry protocols were used to assess NK subsets and NK cytotoxic activity at various time points that included baseline (T1), 6 (T2) and 12 months (T3). Cytokine secretions were measured following mitogenic stimulation of peripheral blood mononuclear cells. RESULTS: NK cytotoxic activity was significantly decreased in the CFS/ME patients at T1, T2 and T3 compared to the non-fatigued group. Additionally, in comparison to the non-fatigued controls, the CFS/ME group had significantly lower numbers of CD56brightCD16- NK cells at both T1 and T2. Interestingly, following mitogenic stimulation, cytokine secretion revealed significant increases in IL-10, IFN-γ and TNF-α at T1 in the CFS/ME group. A significant decrease was observed at T2 in the CFS/ME group for IL-10 and IL-17A while at T3, IL-2 was increased in the CFS/ME group in comparison to the non-fatigued controls. Overall cytotoxic activity was significantly decreased at T3 compared to T1 and T2. CD56brightCD16- NK cells were much lower at T2 compared to T1 and T3. IL-10 and IL-17A secretion was elevated at T2 in comparison to T1 and T3. CONCLUSION: These results confirm decreases in immune function in CFS/ME patients, suggesting an increased susceptibility to viral and other infections. Furthermore, NK cytotoxic activity may be a suitable biomarker for diagnosing CFS/ME as it was consistently decreased during the course of the 12 months study.
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Stress acts on the HPG axis through norepinephrine release into the ovaries, and also inhibits the release of GnRH, luteinizing hormone, estrogen, and progesterone.
“Stress also acts on the HPG axis through norepinephrine release into the ovaries, and also inhibits the release of GnRH, luteinizing hormone, estrogen, and progesterone37.”
From Leveraging Prior Knowledge of Endocrine Immune Regulation in the Therapeutically-relevant Phenotyping of Women with Chronic Fatigue Syndrome (2019) · cites this paper as [37]
The Discussion addresses NK-cell activity and cytokine secretion in CFS/ME, not stress effects on the HPG axis. Searches for norepinephrine release into the ovaries and for stress-related reproductive hormones found no passage addressing GnRH, luteinizing hormone, estrogen, or progesterone. The claim cannot be verified from our copy. (LLM, conf=0.76)
Experimental — accuracy not yet measuredEstrogen has been shown to increase corticotropin secretion in both female monkeys and rats.
“Estrogen for example has been shown to increase corticotropin secretion in both female monkeys and rats37, supporting a feedback loop between the HPG and HPA axes.”
From Leveraging Prior Knowledge of Endocrine Immune Regulation in the Therapeutically-relevant Phenotyping of Women with Chronic Fatigue Syndrome (2019) · cites this paper as [37]
The Results and Discussion passages in our copy concern NK cells and cytokine changes in CFS/ME; no page numbers are available. Searches for estrogen, corticotropin, female monkeys, rats, and HPG/HPA axes found no passage addressing the attributed finding. (LLM, conf=0.76)
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References 60 · Cited by 135
- Authors
- Brenu, E. W., van Driel, M. L., Staines, D. R., Ashton, K. J., Hardcastle, S. L., Keane, J., Tajouri, L., Peterson, D., Ramos, S. B., & Marshall-Gradisnik, S. M.
- Affiliations
- Bond University (AU)
- Corresponding author
- Brenu, Ekua W
- Venue
- Journal of Translational Medicine
- Published
- 2012-05-09
- Volume
- 10
- Issue
- 1
- Pages
- 88-88
- ISSN
- 1479-5876 (ISSN-L)
- PMC
- PMC3464733
- OpenAlex
- W2112732153
- Cited by
- 135
- References
- 60
- Citations by year
- 2026: 4 · 2025: 4 · 2024: 13 · 2023: 10 · 2022: 1 · 2021: 5 · 2020: 4 · 2019: 15 · 2018: 13 · 2017: 8 · 2016: 18 · 2015: 17 · 2014: 7 · 2013: 15 · 2012: 1
- FWCI
- 9.11
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Journal of Translational Medicine (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Bond University Research Portal (Bond University) (submittedVersion, cc-by)
- Griffith Research Online (submittedVersion, cc-by)
- e-publications@bond (Bond University) (submittedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- Judith Jane Mason and Harold Stannett Williams Memorial Foundation
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Fibromyalgia and Chronic Fatigue Syndrome Research
- Life Sciences › Immunology and Microbiology › Immunology › Immune Cell Function and Interaction
- Health Sciences › Medicine › Neurology › Long-Term Effects of COVID-19
- Keywords
- chronic fatigue syndrome, natural killer cells, NK cell subsets, cytokine production, IL-10, IL-17A, interferon-gamma, TNF-α, interleukin-2, immune dysfunction, biomarkers
- MeSH terms
- Adult, Female, Flow Cytometry, Humans, Killer Cells, Natural, Longitudinal Studies, Male, Middle Aged, Fatigue Syndrome, Chronic, Antigens, CD, Case-Control Studies, Immunophenotyping, Cytokines
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