Article: One of the biggest myths about chronic fatigue syndrome just got destroyed

Allyann

Member
http://www.sciencealert.com/one-of-the-biggest-myths-about-chronic-fatigue-syndrome-just-got-destroyed

One of the Biggest Myths About Chronic Fatigue Syndrome Just Got Debunked


Chronic fatigue IS a real disease.
Chronic fatigue syndrome (CFS) or Myalgic Encephalomyelitis (ME) is one of the most perplexing conditions out there. It affects up to 1 million Americans and 2.6 percent of the global population, often triggering exhaustion so severe that patients can't work or study.
But for decades, researchers have struggled to find an underlying cause, leading to an assumption by many doctors that it's 'not a real disease'. Now, Australian researchers have blown that myth wide open, showing for the first time that CFS is linked to a faulty cell receptor in immune cells.
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The latest research has been published in Clinical Experimental Immunology.
 
Last edited:

Seanko

Well-Known Member
The paper is here.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5217865/

Impaired calcium mobilization in natural killer cells from chronic fatigue syndrome/myalgic encephalomyelitis patients is associated with transient receptor potential melastatin 3 ion channels

T. Nguyen,
1 , 2 S. Johnston, 1 , 2 L. Clarke, 1 , 2 P. Smith, 1 D. Staines, 1 , 2 and S. Marshall‐Gradisnik 1 , 2
Author information ► Article notes ► Copyright and License information ►

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SUMMARY

Transient receptor potential melastatin subfamily 3 (TRPM3) ion channels play a role in calcium (Ca2+) cell signalling.

Reduced TRPM3 protein expression has been identified in chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) patients.

However, the significance of TRPM3 and association with intracellular Ca2+ mobilization has yet to be determined.

Fifteen CFS/ME patients (mean age 48·82 ± 9·83 years) and 25 healthy controls (mean age 39·2 ± 12·12 years) were examined. Isolated natural killer (NK) cells were labelled with fluorescent antibodies to determine TRPM3, CD107a and CD69 receptors on CD56dimCD16+NK cells and CD56brightCD16dim/– NK cells. Ca2+ flux and NK cytotoxicity activity was measured under various stimulants, including pregnenolone sulphate (PregS), thapsigargin (TG), 2‐aminoethoxydiphenyl borate (2APB) and ionomycin. Unstimulated CD56brightCD16dim/– NK cells showed significantly reduced TRPM3 receptors in CFS/ME compared with healthy controls (HC).

Ca2+ flux showed no significant difference between groups. Moreover, PregS‐stimulated CD56brightCD16dim/–NK cells showed a significant increase in Ca2+ flux in CFS/ME patients compared with HC. By comparison, unstimulated CD56dimCD16+ NK cells showed no significant difference in both Ca2+ flux and TRPM3 expression.

PregS‐stimulated CD56dimCD16+ NK cells increased TRPM3 expression significantly in CFS/ME, but this was not associated with a significant increase in Ca2+ flux. Furthermore, TG‐stimulated CD56dimCD16+ NK cells increased K562 cell lysis prior to PregS stimulation in CFS/ME patients compared with HC.

Differential expression of TRPM3 and Ca2+ flux between NK cell subtypes may provide evidence for their role in the pathomechanism involving NK cell cytotoxicity activity in CFS/ME.

Keywords: cell surface molecules, inhibitory/activating receptors, natural killer cells
 

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