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ERK1/2, MEK1/2 and p38 downstream signalling molecules impaired in...

Discussion in 'Latest ME/CFS Research' started by Kati, Apr 21, 2016.

  1. Kati

    Kati Patient in training

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    News from NCNED/Griffith University

    NCNED is pleased to announce the release of our latest publication entitled “ERK1/2, MEK1/2 and p38 downstream signalling molecules impaired in CD56dimCD16+ and CD56brightCD16dim/− natural killer cells in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis patients.”

    This paper identifies pathological changes in vital signalling pathways in ME/CFS. These pathways exert a major influence over cell functioning suggesting important fundamental steps in the development of the pathomechanism of ME/CFS. The full article can be accessed by following the link below.

    http://translational-medicine.biomedcentral.com/…/s12967-01…

    We sincerely thank all of our supporters including the Stafford Fox Foundation, Alison Hunter Memorial Foundation, the Mason Foundation, the Queensland Government and all particpants who have contributed to this important research outcome.

    There are more publications to come.

    ERK1/2, MEK1/2 and p38 downstream signalling molecules impaired in CD56dimCD16+ and CD56brightCD16dim/− natural killer cells in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis patient
    Teilah Kathryn Huth, Donald Staines and Sonya Marshall-Gradisnik
    Journal of Translational Medicine201614:97
    DOI: 10.1186/s12967-016-0859-z
    Huth et al. 2016

    Received: 16 September 2015

    Accepted: 10 April 2016

    Published: 21 April 2016



    Abstract
    Background
    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.

    Methods
    Flow cytometric protocols were used to measure phosphorylation of the MAPK pathway in CD56brightCD16dim/− and CD56dimCD16+ 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 CD56brightCD16dim/− and CD56dimCD16+NK cell function using flow cytometric protocols.

    Results
    CFS/ME patients (n = 14) had a significant decrease in ERK1/2 in CD56dimCD16+ NK cells compared to the non-fatigued controls (n = 11) after incubation with K562 cells. CD56brightCD16dim/− NK cells from CFS/ME patients had a significant increase in MEK1/2 and p38 following incubation with K562 cells.

    Conclusions
    This is the first study to report significant differences in MAPK intracellular signalling molecules in CD56dimCD16+ and CD56brightCD16dim/− NK cells from CFS/ME patients. The current results highlight the importance of intracellular signalling through the MAPK pathway for synergistic effector function of CD56dimCD16+ and CD56brightCD16dim/− NK cells to ensure efficient clearance of target cells. In CFS/ME patients, dysfunctional MAPK signalling may contribute to reduced NK cell cytotoxic activity.
     
    RL_sparky, MeSci, Theodore and 7 others like this.
  2. lansbergen

    lansbergen Senior Member

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  3. Snow Leopard

    Snow Leopard Hibernating

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    South Australia
  4. deleder2k

    deleder2k Senior Member

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    https://www.sciencedaily.com/releases/2016/05/160510093906.htm
     
    mango and Kati like this.

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