Journal of IiME Volume 6 Issue 1 (June 2012) in (ME)CFS using a sensitive radioligand assay. They examined serum autoantibodies to recombinant human muscarinic cholinergic receptor 1 (CHRM1) and other receptors in patients with (ME)CFS and the results were compared with those in patients with autoimmune disease and with healthy controls. The mean antiCHRM1 antibody index was significantly higher in patients with (ME)CFS and with autoimmune disease than in controls. Anti-nuclear antibodies were found in 56.7% of patients with (ME)CFS. The patients with positive autoantibodies to CHRM1 had a significantly higher score of ‘feeling muscle weakness’ than negative patients among (ME)CFS patients. The authors conclude: “Autoantibodies to CHRM1 were detected in a large number of (ME)CFS patients and were related to (ME)CFS symptoms. Our findings suggest that subgroups of (ME)CFS are associated with autoimmune abnormalities of CHRM1” (Tanaka S, Kuratsune H et al. Int J Mol Med 2003:12(2):225-230). 2003 Looking at complement activation in (ME)CFS in the light of the need to identify biological markers in (ME)CFS, US researchers used an exercise challenge to induce symptoms of (ME)CFS and to identify a marker that correlated with those symptoms. “Exercise challenge induced significant increases of the complement split product C4a at six hours after exercise only in the (ME)CFS group” (Sorensen B et al. J All Clin Immunol 2003:112(2):397-403). 2003 “(ME)CFS is an increasing medical phenomenon leading to high levels of chronic morbidity. The aim of this study was to screen for changes in gene expression in the lymphocytes of (ME)CFS patients. In a small but well-characterised population of (ME)CFS patients, differential display has been used to clone and sequence genetic markers that are over-expressed in the mononuclear cells of (ME)CFS patients. Many researchers have recognised that current methods of diagnosis lead to the selection of a heterogeneous sample, and these data support that view. It is encouraging that the wide ‘spread’ of data seen in (ME)CFS patients is not seen in the control Invest in ME (Charity Nr. 1114035) samples. The data presented here add weight to the idea that (ME)CFS is a disease characterised by over-expression of genes, some of which are known to be associated with immune system activation. Identifying the triggering events for the induction of these genes will increase our understanding of this disease. Some interesting possibilities include viral infection, neuroendocrine disturbances, and allergen exposure. A link with allergy may be particularly pertinent since approximately 80% of (ME)CFS patients are atopic. Some of the genes identified in this study may therefore be linked with the increase in allergic effects seen in (ME)CFS” (R Powell, S Holgate et al. Clin Exp Allergy 2003:33:1450-1456). 2003 In an Invited Review, Patrick Englebienne from the Department of Nuclear Medicine, Vrije University, Brussels, explained in simple terms the significance of RNase L: “RNase L (2-5oligoadenylate-dependent ribonuclease L) is central to the innate cellular defence mechanism induced by Type I interferons during intracellular infection. In the absence of infection, the protein remains dormant. Recent evidence indicates, however, that the protein is activated in the absence of infection and may play a role in cell differentiation (and) immune activation. A deregulation of this pathway has been documented in immune cells of (ME)CFS patients. This protein escapes the normal regulation (resulting in) a cascade of unwanted cellular events. Recent data indicate that the RNase L system role is not limited to the cell defence mechanism against intracellular infection but extends to the complete innate and adaptive immune systems, including NK and T-cell proliferation and activation, as well as to cell differentiation and proliferation. The presence of unregulated active RNase L fragments in immune cells may lead to deleterious effects which are inherent to the cellular targets of the protein (because) an unregulated destruction of rRNA and of mitochondrial RNA leads to cell apoptosis. Should the RNase L de-regulation exist in muscle cells, it would necessarily restrain normal muscular development and hence activity (and) muscular weakness is a common feature of (ME)CFS” (JCFS 2003:11(2):97-109). www.investinme.org Page 66 of 108

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