Journal of IiME Volume 6 Issue 1 (June 2012) At the CFSAC Science Day meeting on 12th October 2010, Professor Nancy Klimas is reported to have said that chronic immune activation is a key component of the systems imbalance seen in (ME)CFS; that IgG1 and IgG3 are also skewed; that the more symptomatic patients are, the worse their lymphocytes are functioning; that patients with poor NK cell function have less perforin function in their NK cells; that NK cell function is a very good indicator of the severity of the illness; that neuropeptide Y goes up in (ME)CFS patients and it is an important link to the autonomic nervous system – the higher the neuropeptide Y, the more significantly ill patients are, and that neuropeptide Y has links to the cardio-respiratory system and the immune system as well as to other systems; that proinflammatory cytokines are ALL elevated, some more than others, with IL-1  being the most dramatic; that Type 2 cytokines are elevated and are skewed to allergy and autoimmunity; that IL6 is a great biomarker in the (ME)CFS population; that there is a blunted adrenal axis and abnormal serotonin function; that cortisol levels are abnormal and the physiological response to stress in (ME)CFS is very poor (“the connectedness of the endocrine stress response and the immune response is very blunted”); that in (ME)CFS, 25 genes are expressed differently than in healthy controls, but when exercising, one sees many more genes being differently expressed and that exercising is a very, very impressive tool to understand things, as it is an autonomic trigger and that exercise (autonomic stimulus) is enough to inflame pathways; that other diseases with these markers activated include lymphoproliferative disorders and chronic viruses; that (ME)CFS patients are vitamin D deficient and B12 deficient; that(ME)CFS patients have mitochondrial dysfunction; that “we have biomarkers”; that “you can subgroup by symptom and severity”; that “I think I get a pretty good handle on pointing out inflammation with cytokine assays”; that enteroviruses are very important and that “herpes, coxsackie, endogenous viruses – all could reactivate”; that the immune system is a very important player in this disease; that abnormalities seen in the immune system are consistent: immune activation, inflammation, cytokine dysregulation, cellular abnormalities, which are typically seen in infection or autoimmunity (because cytotoxic Tcells are affected, this leans more to infection Invest in ME (Charity Nr. 1114035) than to autoimmunity, but autoimmunity is still an important issue) (http://www.facebook.com/pages/XMRV-GlobalAction/216740433250#!/notes/xmrv-globalaction/here-is-our-close-transcript-of-the-firstpart-of-the-cfsac-science-day/451191706796). 2010 In November 2010 Professor Klimas visited New Zealand on a lecture tour addressing doctors in Auckland, Dunedin and Wellington; the following are from notes taken by a NZ patient with ME, JillNZ, on www.mecfsforums.com. Professor Klimas likes the Canadian Consensus Criteria in preference to the Fukuda criteria because the CCC emphasise post-exertional malaise, which is unique to (ME)CFS; in the last 20 years her team found chronic immune activation (Th2 shift, DR CD26 expression, TNF, IL-1, IL-6) and defects (NK cells, CD8 -- cells do not have enough perforin or granzymes) and macrophages are abnormal: “If you had a chronic virus the immune system would look EXACTLY like this; it doesn’t prove it yet, though, because the pattern is also consistent with an autoimmune problem”; the immune pattern correlates with severity: those with more problems have higher numbers and scores of immune abnormalities; various viruses have been found to be (re)activated – EBV, CMV, HHV6, enteroviruses – all baggage viruses which should remain latent but which have interestingly been found to be activated in (ME)CFS, and something needs to be driving this; we have to remember that blood is not the only reservoir and we need to look at tissue as Chia has shown; a virus does not have to be whole to cause problems; exercise will normally increase cortisol, which acts to control inflammation, but in (ME)CFS, when patients exercise, cortisol goes down and inflammation goes unchecked and gets worse, with pain and delayed autonomic symptoms; the autonomic problems can cause gut motility issues and cerebral perfusion slows down, giving rise to cognitive impairment; her new Dynamic Modelling study looked at 105 patients who used an exercycle for 8 minutes, with blood being drawn at VO2 Max, then again 4 hours later to see all the genes that were turned on and turned off: in (ME)CFS, at VO2 max, it was all the inflammatory cytokines that were turned on (and increased TNF has 80 downstream effects on www.investinme.org Page 89 of 108

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