Journal of IiME Volume 6 Issue 1 (June 2012) start with a conundrum – the name. This is a small point to many academics and clinicians but to sufferers and researchers alike it is at the hub of the enigma in terms of treatment and management and, also, for the researcher in the classification and definition of cohorts – the hallmark of good science….ME is a neurological illness (WHO ICD 10 G93.3) with evidence of immunological and toxicological signs, clear disturbance to the neuro-endocrine stress axis, impairment of the autonomic nervous system, irregularities in perfusion to the brain and indeed to the peripheral vascular system….A review of the literature on the immunology of (ME)CFS (Patarca-Montero R et al: JCFS 2000:6:69-107) reveals that people who have more strictly defined CFS equating with ME have two basic problems with immune function that have been documented by most research groups: 1. immune activation, as demonstrated by elevation of activated T lymphocytes, including cytotoxic T cells, as well as elevations of circulating cytokines, and 2. poor cellular function, with low NK cell cytotoxicity, poor lymphocyte response to mitogens in culture, and frequent immunoglobulin deficiencies, most often IgG1 and IgG3…..Although the causes of ME/CFS remain to be elucidated, many studies provide evidence for abnormalities in immunological markers among patients….Although a subset of patients with immune activation can be identified, serum markers of inflammation and immune activation are said by advocates of the psychiatric aetiology to be of limited diagnostic usefulness in the evaluation of patients with ME/CFS (even though) ME/CFS patients can be categorised by immunological findings….The same psychiatrists carelessly or expediently ignore the increasing evidence for the physical case for ME/CFS” (Research Report in ME/CFS for the Fife Health Board, Scotland. Dr Vance A Spence. November 2000). 2001 The Fifth Biennial International AACFS Research and Clinical Conference was held in Seattle from 26th – 29th January 2001. From the Immunology sessions, the following are highlighted: Professor Kenny De Meirleir (Brussels) presented evidence that a large number of (ME)CFS patients Invest in ME (Charity Nr. 1114035) have an abnormal immune profile; this altered immune system can result in the production of immunologic mediators such as interferons, interleukins and other cytokines. Recently, an up-regulation of the 2-5A Synthetase/RNase L pathway has been shown in (ME)CFS patients, indicating an activated immune state. According to their immununologic profile, patients were divided into three groups and significant differences were found for IFN gamma between groups 2 and 3 and between the controls and group 3. The presence of an increased amount of LMW (low molecular weight) RNase L correlated with higher levels of IFN gamma, which has antiviral properties (Conference Proceedings # 017). Drs K Sugiura, A Komaroff, Eng Tan et al reviewed autoimmunity in (ME)CFS and reported on a multi-centre study. Low titres of antinuclear antibodies have been found in (ME)CFS. The study looked at the presence of autoantibodies to a cellular protein expressed primarily in neuronal cells, MAP2 (a microtubule-associated protein). Initial studies with immunohistochemistry showed a high percentage of (ME)CFS sera reactive to centrosomes. Evidence shows that other proteins besides MAP2 might also be target antigens in (ME)CFS autoimmunity. Of interest was the high frequency of reactors with lupus erythematosus and rheumatoid arthritis compared with (ME)CFS patients (Conference Proceedings #037). Drs Kevin Maher, Nancy Klimas and Mary Ann Fletcher presented on “Flow Cytometric Measurements of Perforin and Natural Killer Cell Activity”: the intracellular content of the Natural Killer (NK) cell is perforin, a cell lytic protein common in many cells of the immune system which correlates with the cytolytic potential of the cell. In (ME)CFS, this chemical is reduced in NK cells. This finding substantiates claims of an NK associated defect in (ME)CFS and suggest a molecular basis for the reduced cytotoxicity (immune system killer cell function). This defect may not be NK specific but may encompass the cytotoxic T cell subset as well. Mice which were genetically engineered to have low or absent levels of perforin showed the same immune abnormalities as (ME)CFS. Other abnormalities www.investinme.org Page 60 of 108
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