Journal of IiME Volume 6 Issue 1 (June 2012) evidence of persisting viral activity, gastrointestinal dysfunction, sleep disruption, pain, cognitive impairment, neuroendocrine dysfunction, genomics (especially the findings of three main abnormalities in ME/CFS, involving the immune system, mitochondrial function and Gprotein signalling: of seven genes up-regulated in ME/CFS, three in particular are notable, these being gelsolin that is involved in apoptosis, one that is upregulated by organophosphates, and the other being a mitochondrial gene that is involved in the demyelination of nerves), and paediatric issues. This conference highlighted the difference between psychiatry and science (http://www.meactionuk.org.uk/Facts_from_Flori da.htm). 2007 On 25th May 2007 the charity ME Research UK (MERUK) hosted an International Research Conference at the Edinburgh Conference Centre, Heriot Watt University, Edinburgh. There were six keynote lectures and eight presentations, with several Question & Answer sessions. The following notes are taken from the keynote lectures and presentations. Items relating to the immunology of ME/CFS include the following: Presentation by Mark Robinson (Department of Applied Physiology, University of Strathclyde): “Response of plasma cytokine IL-6 and its receptors to exercise in ME/CFS” “The physiological role of IL-6 has classically been studied in the context of the immune response, since it is able to exert both pro- and antiinflammatory activities. More recently, IL-6 has been of keen interest to exercise physiologists, with the observation that, even without skeletal muscle damage, plasma levels of this cytokine increase dramatically. In 2000 (researchers) demonstrated that the source of this increased IL-6 can almost exclusively be attributed to the working of skeletal muscle, where it is both produced and subsequently released”. “Exercise-induced IL-6 in the muscle acts in a hormone-like manner, helping to maintain the fuel Invest in ME (Charity Nr. 1114035) homeostasis during exercise and when skeletal muscle glycogen levels become depleted”. “The main finding of the study was a clear trend towards a lower resting level of the soluble IL-6 receptor in ME/CFS patients”. Keynote Lecture by Professor Nancy Klimas (University of Miami): “The Immunology of ME/CFS”. Nancy Klimas, Professor of Medicine & Immunology at the University of Miami and worldrenowned expert on the immunology of ME/CFS, delivered a compelling keynote lecture. She said there is a real genetic component in ME/CFS (HLA-DR, which predisposes to autoimmune illness). She stressed the findings of an Australian study which found that the severity of the initial infection is the single predictor of perpetuation of ME/CFS and that there is no psychological component in its perpetuation. Professor Klimas explained the imbalance seen in ME/CFS between Type I and Type II cytokines: in ME/CFS they see a lot of Type II cytokine expression, which means there is an inhibition of Type I expression, which in turn triggers the inflammatory cascade of tumour necrosis factor (TNF), IL-6 and IL-1. This is important, because Type I cytokines are needed for the function of cytolytic T cells and NK cells are part of the whole immune mechanism, which is being inhibited in ME/CFS. She pointed out that what has been seen over many years of research by many different groups is (quote) “a lot of evidence of this chronic immune activation, looking at expression of activation markers on the cells, looking at cytokine levels, looking at cytokine expression. The consequence, or may be a part of this, is a lot of functional abnormalities of cytotoxic T cells and NK cells, macrophage abnormalities, antibody production abnormalities and neutrophil abnormalities. NK cell function is very poor—NK cells should kill in a certain unit of time: in normals this is 30-40% in four hours, but in ME/CFS it is half of that”. www.investinme.org Page 77 of 108
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