Journal of IiME Volume 6 Issue 1 (June 2012) supported a formal change to ‘chronic fatigue and immune dysfunction syndrome’ in recognition of the various immune abnormalities documented by private and public-sector researchers….Dr Klimas presented Dr Reeves with a notebook filled with medical articles on the immune abnormalities found in CFIDS in defence of this recommendation”. During those meetings, Dr Phillip Peterson acknowledged the immune system abnormalities and the adequacy of evidence to support immunotherapy, stating that he had found no other disease with such global immune disturbance (The CFIDS Chronicle, November 1993 and Winter [January] 1994). 1994 An International Meeting on (ME) Chronic Fatigue Syndrome was held in Dublin on 18th-20th May 1994 under the auspices of the World Federation of Neurology. Professor Dr Rainer Ihle from Germany said that data on 375 (ME)CFS patients demonstrated various immunological changes and autoantibodies (especially antinuclear antibody and microsomal thyroid antibodies) in an abnormally large proportion of patients, suggesting impaired immunity and facilitating transition to autoimmune disease (“On the basis of these immunological serological and organspecific findings, which affirm previously published results, it would appear that the organic nature of the pathogenesis of (ME)CFS has now been demonstrated”). Dr Jay Levy from San Francisco presented serological and immunological data from (ME)CFS patients, pointing out that, by lymphocyte phenotype analysis, the T8 suppressor subset was decreased, a notable and important finding. He also found that activated T cells were increased, with the most pronounced increases seen in the sickest patients, and that NK cell activity and cytotoxic lymphocyte activity were both depressed in (ME)CFS patients. 1994 Invest in ME (Charity Nr. 1114035) “The up-regulated 2-5A pathway in (ME)CFS is consistent with an activated immune state and a role for persistent viral infection in the pathogenesis of (ME)CFS. The object of this study was to measure key parameters of the 2-5A synthetase/RNase-L antiviral pathway in order to evaluate possible viral involvement in (ME)CFS. The data presented suggest that 2-5A synthetase/RNase L pathway is an important biochemical indicator of the anti-viral state in (ME)CFS. Evidence that this pathway is activated in (ME)CFS was identified in this subset of severely disabled individuals as related to virological and immunologic status. This pathway phenotype could result from chronic overstimulation due to chronic viral reactivation” (RJ Suhadolnik et al. Clin Inf Dis 1994:18(Suppl 1):S96S104). 1994 “Controlled studies of T cells in patients with (ME)CFS have (shown that) the three most prominent and apparently reproducible findings for (ME)CFS patients are as follows (1) Impaired lymphocyte proliferation in response to stimulation…has been repeatedly documented and also has been shown to be dissociated from the potential effect of concurrent mood disturbance on this response. (2) …several investigators have reported increased numbers of peripheral blood lymphocytes bearing activation markers (such as HLA-DR and interleukin-2R) in these patients. (3) Impaired cell-mediated immune function in vivo is suggested by reports of an increased number of reduced or absent DTH (delayed-type hypersensitivity) skin testing responses in patients with (ME)CFS” (AR Lloyd. Clin Inf Dis 1994:18: (Suppl 1): S134-5). 1994 “Compared with those of healthy individuals, patients’ CD8+ T cells expressed reduced levels of CD11b and expressed the activation markers CD38 and HLA-DR at elevated levels…These findings indicate expansion of a population of activated CD8+ cytotoxic T lymphocytes. A marked decrease in NK cell activity was found in almost all patients with (ME)CFS, as compared with that in healthy controls…The results of this study suggest that immune cell phenotype changes and NK cell www.investinme.org Page 45 of 108

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