scholarly journals Dysregulation of Protein Kinase Gene Expression in NK Cells from Chronic Fatigue Syndrome/Myalgic Encephalomyelitis Patients

2016 ◽  
Vol 10 ◽  
pp. GRSB.S40036
Author(s):  
Anu Chacko ◽  
Donald R. Staines ◽  
Samantha C. Johnston ◽  
Sonya M. Marshall-Gradisnik
2008 ◽  
Vol 197 (8) ◽  
pp. 1171-1184 ◽  
Author(s):  
Jonathan R. Kerr ◽  
Robert Petty ◽  
Beverley Burke ◽  
John Gough ◽  
David Fear ◽  
...  

2014 ◽  
Vol 67 (12) ◽  
pp. 1078-1083 ◽  
Author(s):  
Nana Shimosako ◽  
Jonathan R Kerr

AimsWe have reported gene expression changes in patients with chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) and the fact that such gene expression data can be used to identify subtypes of CFS/ME with distinct clinical phenotypes. Due to the difficulties in using a comparative gene expression method as an aid to CFS/ME disease and subtype-specific diagnosis, we have attempted to develop such a method based on single-nucleotide polymorphism (SNP) analysis.MethodsTo identify SNP allele associations with CFS/ME and CFS/ME subtypes, we tested genomic DNA of patients with CFS/ME (n=108), patients with endogenous depression (n=17) and normal blood donors (n=68) for 504 human SNP alleles located within 88 CFS-associated human genes using the SNP Genotyping GoldenGate Assay (Illumina, San Diego, California, USA). 360 ancestry informative markers (AIM) were also examined.Results21 SNPs were significantly associated with CFS/ME compared with depression and normal groups. 148 SNP alleles had a significant association with one or more CFS/ME subtypes. For each subtype, associated SNPs tended to be grouped together within particular genes. AIM SNPs indicated that 4 subjects were of Asian origin while the remainder were Caucasian. Hierarchical clustering of AIM data revealed the relatedness between 2 couples of patients with CFS only and confirmed the overall heterogeneity of all subjects.ConclusionsThis study provides evidence that human SNPs located within CFS/ME associated genes are associated with particular genomic subtypes of CFS/ME. Further work is required to develop this into a clinically useful subtype-specific diagnostic test.


2013 ◽  
Vol 04 (03) ◽  
pp. 165-170
Author(s):  
Ekua W. Brenu ◽  
Gunn M. Atkinson ◽  
Mieke L. van Driel ◽  
Sanne Kreijkamp-Kaspers ◽  
Don R. Staines ◽  
...  

Author(s):  
Stanley Du Preez ◽  
Natalie Eaton-Fitch ◽  
Helene Cabanas ◽  
Donald Staines ◽  
Sonya Marshall-Gradisnik

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a complex multisystemic disorder responsible for significant disability. Although a unifying etiology for ME/CFS is uncertain, impaired natural killer (NK) cell cytotoxicity represents a consistent and measurable feature of this disorder. Research utilizing patient-derived NK cells has implicated dysregulated calcium (Ca2+) signaling, dysfunction of the phosphatidylinositol-4,5-bisphosphate (PIP2)-dependent cation channel, transient receptor potential melastatin (TRPM) 3, as well as altered surface expression patterns of TRPM3 and TRPM2 in the pathophysiology of ME/CFS. TRPM7 is a related channel that is modulated by PIP2 and participates in Ca2+ signaling. Though TRPM7 is expressed on NK cells, the role of TRPM7 with IL-2 and intracellular signaling mechanisms in the NK cells of ME/CFS patients is unknown. This study examined the effect of IL-2 stimulation and TRPM7 pharmacomodulation on NK cell cytotoxicity using flow cytometric assays as well as co-localization of TRPM7 with PIP2 and cortical actin using confocal microscopy in 17 ME/CFS patients and 17 age- and sex-matched healthy controls. The outcomes of this investigation are preliminary and indicate that crosstalk between IL-2 and TRMP7 exists. A larger sample size to confirm these findings and characterization of TRPM7 in ME/CFS using other experimental modalities are warranted.


2019 ◽  
Vol 41 (5) ◽  
pp. 815-835.e6 ◽  
Author(s):  
Mary G. Jeffrey ◽  
Lubov Nathanson ◽  
Kristina Aenlle ◽  
Zachary M. Barnes ◽  
Mirza Baig ◽  
...  

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