NK cells are the most consistent test I've had over a long time period, so I like using these tests to 'prove' I am ill, when doctors remind me ''you don't have a temperature''. (One of the first signs of ME/Chronic Lyme in many, is the loss of normal fevers - that raise core temperature and kill pathogens). What do most PWME CFS have? Lower body core temperature....infections love that.
I also point out my Interferon Gamma (IFN-g) is many times elevated and the IFN-a is reduced (antiviral) Combined, this implies chronic infection especially if you go even more complicated (as I like to) and see I lack antibodies to common infections I should have, that I don't because my immune system 'forgot' - this phenomena is seen in some immunosupressive disorders.
This then makes some sense if we look at Science.........and then link to
LPS and LPS to ME CFS/Lyme...
The generation of IFN-gamma by PBMC after treatment with LPS strongly suggests that the enhancement of NK cell activity may be indirectly due to IFN production.
Source:
Immunology. 1991 Aug;73(4):450-6.
Activation of human natural killer cells by lipopolysaccharide and generation of interleukin-1 alpha, beta, tumour necrosis factor and interleukin-6. Effect of IL-1 receptor antagonist.
Conti P1, Dempsey RA, Reale M, Barbacane RC, Panara MR, Bongrazio M, Mier JW.
11 years later...... they comment that Cytokines regulate LPS and IFN....
NK cells and NKT cells are the most abundant IFN-gamma-producing cells in the mouse spleen after LPS challenge and that IL-10 and IL-12 are key functional regulators of LPS-induced IFN-gamma production.
Source:
Clin Diagn Lab Immunol. 2002 May;9(3):530-43.
Endotoxin-induced gamma interferon production: contributing cell types and key regulatory factors.
Varma TK1, Lin CY, Toliver-Kinsky TE, Sherwood ER.
And my Cytokines are also very high....again, consistently and mine don't vanish after 3 years.
The reality is ME can lead to serious other secondary disorders like Cancer, life threatening allergic reactions and heart failure and isn't a syndrome of 'fatigue'. So we need to really ignore this issue and focus on actual patients with ME rather than patients who met criteria for 'fatigue' (as it won't get us anywhere and never has in 25 years).
This requires chronic immune activation, inflammation likely driven by autoimmunity (from infection) - never looked at, due to the CDC creating CFS and focusing on fatigue, never researching severe cohorts, sick for years and years with all this co-morbidity that leads to removal from from CFS research - that's how you hide ME.
So regarding ME and researching ME....there is some ideas
that via Lyme, some forms of Autism is linked to a chronic low grade sepsis (blood poisoning), naturally not acute or the patients would be dead within a day. Something, 'novel' then, but what? (NB: Inflammatory profiles in some cases of Autism appear to be identical to CFS).
From looking at Kenny De Meirleir's research (and others regarding LPS in CFS) it looks like we might be getting 'translocation' of bacteria from the stomach to other organs, maybe even our CNS and likely our lymphatic system. This would then make sense why you find in ME, not CDC Syndrome, such high Cytokines and it would make even more sense when you exercise, these Cytokines will go crazy (as shown by Dr Nancy Klimas) when patients are on exercise bikes who are moderately affected but biologically ill.
Ergo GET and CBT is not only fradulent (PACE trial) it's potentially DANGEROUS to exercise when infected, IF, the heart muscle is involved.
If research can demonstrate what is special about
LPS in ME CFS (e.g. from Bartonella etc), which by the way infects endothelium (VEGF and TGF-B1 can be elevated in ME/Lyme patients). VEGF is a growth factor associated to this part of the body (blood vessels), then it may be a big breakthrough to then tie this to Dr Ron Davis's work (and his team) because we already know from Jonas Blomberg, that Mitochondria is affected by infection (antibodies to heat shock proteins) - mitochondrial by Chlamydia Pneumoniae (Lyme co infection) in almost 1 in 4 of the ME sufferers tested.
IgM to specific cross-reactive epitopes of human and microbial HSP60 occurs in a subset of ME, compatible with infection-induced autoimmunity.
Source:
PLoS One. 2013 Nov 28;8(11):e81155. doi: 10.1371/journal.pone.0081155. eCollection 2013.
Epitopes of microbial and human heat shock protein 60 and their recognition in myalgic encephalomyelitis.
Elfaitouri A1, Herrmann B, Bölin-Wiener A, Wang Y, Gottfries CG, Zachrisson O, Pipkorn R, Rönnblom L, Blomberg J.
And it would then make potential sense this all ties in with
NK Cells 'phenomena' in ME CFS and would help create subsets of infected autoimmune patients who have 'it' and who don't, and if they don't, there is another reason and that can be researched or explained by another pathway. So everyone would benefit from subgrouping.
