Journal of IiME Volume 6 Issue 1 (June 2012) event…” (Bellanti JA et al. Allergy Asthma Proc 2005:26(1):19-28). 2005 “Arguments exist as to the cause of (ME)CFS. Some think that it is an example of symptom amplification indicative of psychogenic illness, while our group thinks that some (ME)CFS patients may have brain dysfunction. We did spinal taps (lumbar puncture) on (ME)CFS patients. We found that significantly more (ME)CFS patients had elevations either in protein levels or numbers of cells than healthy controls and (some) patients had protein levels and cell numbers that were higher than laboratory norms. In addition, of the 11 cytokines detectable in spinal fluid, (some) were lower in patients than in controls (and some) were higher in patients. The results support two hypotheses: that some (ME)CFS patients have a neurological abnormality and that immune dysregulation within the central nervous system may be involved in this process. A recent study showing elevations of IL-8 and IL-10 levels during chemotherapy-induced symptoms resembling some of those seen in (ME)CFS provides additional evidence for this hypothesis” (Benjamin H Natelson et al. Clin Diagn Lab Immunol 2005:12(1):52-55). 2005 An article in The Scientist pointed out the need to measure cytokines in diverse disorders: “The immune system is often likened to the military. The body’s army has weapons such as antibodies and complement, and soldiers such as macrophages and natural killer cells. The immune system sports an impressive communications infrastructure in the form of intracellular protein messengers called cytokines and the cellular receptors that recognise them. The cytokine family consists of such soluble growth factors as the interleukins, interferons, and tumour necrosis factor, among others. Their measurement has become an integral part of both clinical diagnostics and biomedical research” (JP Roberts. The Scientist 2005:19:3:30). It needs to be noted that in the UK, the NICE Clinical Guideline 53 on “CFS” (2007) proscribes such measurements in people with ME/CFS, as did Invest in ME (Charity Nr. 1114035) the MRC’s “CFS/ME Research Advisory Group Research Strategy” Report of 1st May 2003, as did the CMO’s Report of 2002, and as did the Joint Royal Colleges Report (CR54) of 1996. 2005 “Hyperactivation of an unwanted cellular cascade by the immune-related protein RNase L has been linked to reduced exercise capacity in persons with (ME)CFS. This investigation compares exercise capabilities of (ME)CFS patients with deregulation of the RNase L pathway and CFS patients with normal regulation. The results implicate abnormal immune activity in the pathology of exercise intolerance in (ME)CFS and are consistent with a channelopathy involving oxidative stress and nitric-oxide toxicity” (Snell CR et al. In Vivo 2005:19(2):387-390). 2005 “Diminished NK cell cytotoxicity is a frequently reported finding (in ME/CFS). However, the molecular basis of this defect has not been described. Perforin is a protein found within intracellular granules of NK and cytotoxic T cells. Quantitative fluorescence flow cytometry was used to the intracellular perforin content in (ME)CFS subjects and healthy controls. A significant reduction in the NK cell associated perforin levels in samples from (ME)CFS patients compared to healthy controls was observed. There was also an indication of a reduced perforin level within the cytotoxic T cells of (ME)CFS subjects, providing the first evidence (of) a T cell associated cytotoxic deficit in (ME)CFS. Because perforin is important in immune surveillance and homeostatis of the immune system, its deficiency may prove to be an important factor in the pathogenesis of (ME)CFS and its analysis may prove useful as a biomarker in the study of (ME)CFS” (Maher KJ, Klimas NG, Fletcher MA. Clin Exp Immunol 2005:142(3):505511). 2005 “Previous research has shown that patients with (ME)CFS present with an abnormal exercise response and exacerbations of symptoms after www.investinme.org Page 71 of 108
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