Journal of IiME Volume 6 Issue 1 (June 2012) another investigator (Professor Suhadolnik from the US), lending credibility to the result” (Am J Med 2000:108:169-171). (Belgian research has focused on the abnormal enzyme pathways and 88% of (ME)CFS patients tested positive for RNase L. The 37kDa is produced by calpain cleavage, and the whole process affects the calcium and potassium ion channel mechanisms. RNase L is a likely marker for (ME)CFS and correlates with severity. It is negative in AIDS -- with acknowledgement to Dr Rosamund Vallings). 2000 “Blood and lymph nodes samples were obtained from patients with (ME)CFS. While a greater proportion of T lymphocytes from both lymph nodes and peripheral blood of (ME)CFS patients are immunologically naïve, the proportions of lymphocytes with a memory phenotype predominate in lymph nodes and peripheral blood of (ME)CFS patients. (ME)CFS has been proposed to be a disease of autoimmune aetiology and in this respect it is interesting to note that decreased proportions of CD45RA+T (naïve) cells are also seen in the peripheral blood of patients with autoimmune diseases” (Mary Ann Fletcher, Nancy Klimas et al. JCFS 2000:7(3):65-75). 2000 A major and detailed Review of the immunology of (ME)CFS was published by internationallyrenowned immunologists Professors Robert Patarca and Nancy Klimas, together with the distinguished long-time ME/CFS research immunologist Professor Mary Ann Fletcher. It contains 212 references. It is clear that people with (ME)CFS have two basic problems with immune function: (1) immune activation and (2) poor cellular function. These findings have a waxing and waning temporal pattern consistent with episodic immune dysfunction. The interplay of these factors can account for the perpetuation of (ME)CFS with remission/exacerbation cycles. The Review considers the evidence of immune cell phenotypic distributions; immune cell function; cytokines and other soluble immune mediators; immunoglobulins; autoantibodies; circulating Invest in ME (Charity Nr. 1114035) immune complexes; Type I to Type II cytokine shift and the relationship between stressors, cytokines and symptoms. The data summarised indicate that (ME)CFS is associated with immune abnormalities that can account for the physiopathological symptomatology, and recommends that future research should further elucidate the cellular basis for immune dysfunction in (ME)CFS and its implications (JCFS 2000:6(3/4):69-107). 2000 The US National Institutes of Health held a State of the Science Conference on (ME)CFS on 23rd-24th October 2000 in Arlington, Virginia, and was attended by more than 200 people. The conference was divided into six topic areas: neuroendocrinology, neurocognition, pain, immunology, fatigue and orthostatic intolerance. Panelists included well-known (ME)CFIDS physicians such as Drs Nancy Klimas, David Bell, Dedra Buchwald and Peter Rowe. The Immunology section was described in the UK ME Association’s magazine “Perspectives” (Spring 2001) as the most interesting. It was noted that (i) previous studies suggested that the immune system and immune modulators (the chemical cascade that stimulates the immune system to act) are involved in the process of the illness; (ii) HLA markers are more common in (ME)CFS patients and these markers could be associated with autoimmune disease; (iii) the chemicals of the immune system may be directly or indirectly linked to symptom expression; (iv) NK function is low; (v) some classes of IgG are low; (vi) a CD3 receptor may have reduced expression in (ME)CFS patients; (vii) there is a shift during the illness from cellmediated immunity to humoral immunity (antibody-based), and this pattern is associated with autoimmune disease and chronic infection. The conference concluded with the expert panel summarising (ME)CFIDS research needs, most notably that researchers must subgroup patients by unique features such as immunology. 2000 “There is now so much literature from so many varying aspects of biology in ME/CFS that it is simply not possible to summarise it all in a paragraph or two. By calling the illness CFS we www.investinme.org Page 59 of 108
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