Journal of IiME Volume 6 Issue 1 (June 2012) numbers…and thereby activate lymphocytic dendritic cells that reside in the brain, particularly microglia and perivascular cells, and this state of low-level activation can last decades. Activated microglia, like macrophages, secrete proinflammatory cytokines (e.g. TNF, IL-1) and NO (nitric oxide). There is increased neutrophil apoptosis in (ME)CFS”. Professor Robert Suhadolnik (Temple University, Philadelphia) reviewed the evidence and effect of the up-regulated 2-5A synthetase RNase L antiviral defence pathway. There is a 500-fold excess of bioactive 2-5A in (ME)CFS. The higher the RNase L activity, the lower the patient’s ability to function. These patients also have a low molecular weight 37 kDa RNase L which is not found in healthy controls, patients with depression, or fibromyalgia patients. The patient has lowered signal transduction, lowered cell proliferation, lowered ATP production, lowered cellular metabolism, lowered protein synthesis, impaired NK cell function, abnormal exercise response, loss of potassium from muscle, abnormal sodium retention, hyperventilation, central fatigue, sleep disturbances, and muscle cramps and weakness. Dr Kevin Maher (University of Miami) presented evidence that “key proteins associated with the cytolytic process (granzymes A and B) are present at lower cellular concentrations in NK cells from individuals with (ME)CFS”. Dr Jo Nijs (Belgium) presented evidence for an association between intracellular (elastase activity) immune dysregulation and impairments in cardio-respiratory fitness in (ME)CFS patients. This study indicates subtle underlying lung damage. (A presentation by Dr Anna GarciaQuintana from Spain showed that the average maximal oxygen uptake of (ME)CFS patients was only 15.2, whereas the sedentary controls’ uptake was 25.9, and the physically active controls’ uptake was 66.6). Professors Nancy Klimas and Leonard Jason discussed sub-grouping, concluding that finding distinct sub-populations has clear clinical implications by defining groups for targeted Invest in ME (Charity Nr. 1114035) intervention. Objective measures are needed for this approach and can include issues such as immune disturbance (cytokines, cell function). “Sub-grouping is the key to understanding how (ME)CFS begins, how it is maintained, how medical and psychological variables influence its course and how it can be prevented, treated and cured”. In her summary Professor Klimas noted that all the reports confirmed and augmented the same cycle of immunological and neurological malfunctions but said that there is a risk of (ME)CFS being defined as a behavioural disorder if (biomedical) research is not supported (with grateful acknowledgement to Paula Carnes, Dr Rosamund Vallings and Dr Charles Lapp). 2005 In her Incoming Presidential Address for the AACFS, immunologist Professor Nancy Klimas said: “I am proud to assume the role of president of the AACFS, an organisation with a pressing and compelling mission. The AACFS exists to promote research, education, and advocacy to further our understanding and eventually develop effective treatments for this disabling illness….Our patients are terribly ill, misunderstood, and suffer at the hands of a poorly informed medical establishment and society” (Co-Cure ACT: 21st March 2005). 2005 “There are a group of diseases that the allergistimmunologist may be called up to manage…that appear to be initiated by allergic mechanisms….In patients with (ME)CFS, there appears to be a fundamental dysfunction of the neuroendocrineimmunological system with deficiencies of immunological and neurological function which, together with chronic viral infection, may lead to a sequence of events responsible for the symptoms of this disorder….An understanding of the interactive responses involved in the neuroendocrine-immunological network is essential for a comprehension of the pathophysiology of…(ME)CFS…and the role of allergies appears to be an important triggering www.investinme.org Page 70 of 108
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