PMID- 27727448
OWN - NLM
STAT- MEDLINE
DCOM- 20170509
LR  - 20181113
IS  - 1365-2249 (Electronic)
IS  - 0009-9104 (Print)
IS  - 0009-9104 (Linking)
VI  - 187
IP  - 2
DP  - 2017 Feb
TI  - Impaired calcium mobilization in natural killer cells from chronic fatigue 
      syndrome/myalgic encephalomyelitis patients is associated with transient receptor 
      potential melastatin 3 ion channels.
PG  - 284-293
LID - 10.1111/cei.12882 [doi]
AB  - Transient receptor potential melastatin subfamily 3 (TRPM3) ion channels play a 
      role in calcium (Ca(2+) ) 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 
      Ca(2+) 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 CD56(dim) CD16(+) NK 
      cells and CD56(bright) CD16(dim/-) NK cells. Ca(2+) flux and NK cytotoxicity 
      activity was measured under various stimulants, including pregnenolone sulphate 
      (PregS), thapsigargin (TG), 2-aminoethoxydiphenyl borate (2APB) and ionomycin. 
      Unstimulated CD56(bright) CD16(dim/-) NK cells showed significantly reduced TRPM3 
      receptors in CFS/ME compared with healthy controls (HC). Ca(2+) flux showed no 
      significant difference between groups. Moreover, PregS-stimulated CD56(bright) 
      CD16(dim/-) NK cells showed a significant increase in Ca(2+) flux in CFS/ME 
      patients compared with HC. By comparison, unstimulated CD56(dim) CD16(+) NK cells 
      showed no significant difference in both Ca(2+) flux and TRPM3 expression. 
      PregS-stimulated CD56(dim) CD16(+) NK cells increased TRPM3 expression 
      significantly in CFS/ME, but this was not associated with a significant increase 
      in Ca(2+) flux. Furthermore, TG-stimulated CD56(dim) CD16(+) NK cells increased 
      K562 cell lysis prior to PregS stimulation in CFS/ME patients compared with HC. 
      Differential expression of TRPM3 and Ca(2+) flux between NK cell subtypes may 
      provide evidence for their role in the pathomechanism involving NK cell 
      cytotoxicity activity in CFS/ME.
CI  - (c) 2016 The Authors. Clinical & Experimental Immunology published by John Wiley & 
      Sons Ltd on behalf of British Society for Immunology.
FAU - Nguyen, T
AU  - Nguyen T
AD  - The National Centre for Neuroimmunology and Emerging Diseases, Menzies Health 
      Institute, Gold Coast, QLD, Australia.
AD  - School of Medical Science, Griffith University, Gold Coast, QLD, Australia.
FAU - Johnston, S
AU  - Johnston S
AD  - The National Centre for Neuroimmunology and Emerging Diseases, Menzies Health 
      Institute, Gold Coast, QLD, Australia.
AD  - School of Medical Science, Griffith University, Gold Coast, QLD, Australia.
FAU - Clarke, L
AU  - Clarke L
AD  - The National Centre for Neuroimmunology and Emerging Diseases, Menzies Health 
      Institute, Gold Coast, QLD, Australia.
AD  - School of Medical Science, Griffith University, Gold Coast, QLD, Australia.
FAU - Smith, P
AU  - Smith P
AD  - The National Centre for Neuroimmunology and Emerging Diseases, Menzies Health 
      Institute, Gold Coast, QLD, Australia.
FAU - Staines, D
AU  - Staines D
AD  - The National Centre for Neuroimmunology and Emerging Diseases, Menzies Health 
      Institute, Gold Coast, QLD, Australia.
AD  - School of Medical Science, Griffith University, Gold Coast, QLD, Australia.
FAU - Marshall-Gradisnik, S
AU  - Marshall-Gradisnik S
AD  - The National Centre for Neuroimmunology and Emerging Diseases, Menzies Health 
      Institute, Gold Coast, QLD, Australia.
AD  - School of Medical Science, Griffith University, Gold Coast, QLD, Australia.
LA  - eng
PT  - Journal Article
DEP - 20161123
PL  - England
TA  - Clin Exp Immunol
JT  - Clinical and experimental immunology
JID - 0057202
RN  - 0 (CD56 Antigen)
RN  - 0 (Receptors, IgG)
RN  - 0 (TRPM Cation Channels)
RN  - 0 (TRPM3 protein, human)
RN  - 04Y4D91RG0 (pregnenolone sulfate)
RN  - 67526-95-8 (Thapsigargin)
RN  - 73R90F7MQ8 (Pregnenolone)
SB  - IM
MH  - Adult
MH  - CD56 Antigen/metabolism
MH  - Calcium Signaling
MH  - Cytotoxicity, Immunologic
MH  - Fatigue Syndrome, Chronic/*genetics
MH  - Female
MH  - Humans
MH  - K562 Cells
MH  - Killer Cells, Natural/*physiology
MH  - Male
MH  - Middle Aged
MH  - Pregnenolone/metabolism
MH  - Receptors, IgG/metabolism
MH  - TRPM Cation Channels/*genetics
MH  - Thapsigargin/metabolism
PMC - PMC5217865
OTO - NOTNLM
OT  - cell surface molecules
OT  - inhibitory/activating receptors
OT  - natural killer cells
EDAT- 2016/10/12 06:00
MHDA- 2017/05/10 06:00
PMCR- 2016/11/23
CRDT- 2016/10/12 06:00
PHST- 2016/08/12 00:00 [received]
PHST- 2016/09/22 00:00 [revised]
PHST- 2016/10/03 00:00 [accepted]
PHST- 2016/10/12 06:00 [pubmed]
PHST- 2017/05/10 06:00 [medline]
PHST- 2016/10/12 06:00 [entrez]
PHST- 2016/11/23 00:00 [pmc-release]
AID - CEI12882 [pii]
AID - 10.1111/cei.12882 [doi]
PST - ppublish
SO  - Clin Exp Immunol. 2017 Feb;187(2):284-293. doi: 10.1111/cei.12882. Epub 2016 Nov 
      23.