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ERK1/2, MEK1/2 and p38 downstream signalling molecules impaired in CD56dimCD16+ and CD56brightCD16dim/− natural killer cells in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis patients

Overview of attention for article published in Journal of Translational Medicine, April 2016
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About this Attention Score

  • In the top 5% of all research outputs scored by Altmetric
  • High Attention Score compared to outputs of the same age (96th percentile)
  • High Attention Score compared to outputs of the same age and source (96th percentile)

Mentioned by

news
6 news outlets
twitter
21 X users
facebook
9 Facebook pages
wikipedia
1 Wikipedia page

Citations

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32 Dimensions

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58 Mendeley
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Title
ERK1/2, MEK1/2 and p38 downstream signalling molecules impaired in CD56dimCD16+ and CD56brightCD16dim/− natural killer cells in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis patients
Published in
Journal of Translational Medicine, April 2016
DOI 10.1186/s12967-016-0859-z
Pubmed ID
Authors

Teilah Kathryn Huth, Donald Staines, Sonya Marshall-Gradisnik

Abstract

Natural Killer (NK) cell effector functions are dependent on phosphorylation of the mitogen-activated protein kinases (MAPK) pathway to produce an effective immune response for the clearance of target cells infected with viruses, bacteria or malignantly transformed cells. Intracellular signals activating NK cell cytokine production and cytotoxic activity are propagated through protein phosphorylation of MAPKs including MEK1/2, ERK1/2, p38 and JNK. Reduced NK cell cytotoxic activity is consistently reported in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME) patients and intracellular signalling by MAPK in NK cells remains to be investigated. Therefore, the purpose of this paper was to investigate MAPK downstream signalling molecules in NK cell phenotypes from CFS/ME patients. Flow cytometric protocols were used to measure phosphorylation of the MAPK pathway in CD56(bright)CD16(dim/-) and CD56(dim)CD16(+) NK cells following stimulation with K562 tumour cells or phorbol-12-myristate-13-acetate plus ionomycin. NK cell cytotoxic activity, degranulation, lytic proteins and cytokine production were also measured as markers for CD56(bright)CD16(dim/-) and CD56(dim)CD16(+) NK cell function using flow cytometric protocols. CFS/ME patients (n = 14) had a significant decrease in ERK1/2 in CD56(dim)CD16(+) NK cells compared to the non-fatigued controls (n = 11) after incubation with K562 cells. CD56(bright)CD16(dim/-) NK cells from CFS/ME patients had a significant increase in MEK1/2 and p38 following incubation with K562 cells. This is the first study to report significant differences in MAPK intracellular signalling molecules in CD56(dim)CD16(+) and CD56(bright)CD16(dim/-) NK cells from CFS/ME patients. The current results highlight the importance of intracellular signalling through the MAPK pathway for synergistic effector function of CD56(dim)CD16(+) and CD56(bright)CD16(dim/-) NK cells to ensure efficient clearance of target cells. In CFS/ME patients, dysfunctional MAPK signalling may contribute to reduced NK cell cytotoxic activity.

X Demographics

X Demographics

The data shown below were collected from the profiles of 21 X users who shared this research output. Click here to find out more about how the information was compiled.
Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 58 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
United Kingdom 1 2%
Norway 1 2%
Unknown 56 97%

Demographic breakdown

Readers by professional status Count As %
Researcher 11 19%
Student > Doctoral Student 6 10%
Other 5 9%
Student > Ph. D. Student 5 9%
Student > Master 5 9%
Other 10 17%
Unknown 16 28%
Readers by discipline Count As %
Medicine and Dentistry 10 17%
Immunology and Microbiology 9 16%
Agricultural and Biological Sciences 7 12%
Biochemistry, Genetics and Molecular Biology 6 10%
Psychology 3 5%
Other 6 10%
Unknown 17 29%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 62. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 20 February 2017.
All research outputs
#671,848
of 25,019,915 outputs
Outputs from Journal of Translational Medicine
#135
of 4,539 outputs
Outputs of similar age
#12,123
of 305,365 outputs
Outputs of similar age from Journal of Translational Medicine
#4
of 90 outputs
Altmetric has tracked 25,019,915 research outputs across all sources so far. Compared to these this one has done particularly well and is in the 97th percentile: it's in the top 5% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 4,539 research outputs from this source. They typically receive a lot more attention than average, with a mean Attention Score of 10.8. This one has done particularly well, scoring higher than 97% of its peers.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 305,365 tracked outputs that were published within six weeks on either side of this one in any source. This one has done particularly well, scoring higher than 96% of its contemporaries.
We're also able to compare this research output to 90 others from the same source and published within six weeks on either side of this one. This one has done particularly well, scoring higher than 96% of its contemporaries.