dipeptidyl peptidase IV. PLoS ONE 2010; 5: e10817. Journal of IiME Volume 6 Issue 1 (June 2012) 377–85. 7. Mihaylova I, DeRuyter M, Rummens JL, Basmans E, Maes M. Decreased expression of CD69 in chronic fatigue syndrome in relation to inflammatory markers: evidence for a severe disorder in the early activation of T lymphocytes and natural killer cells. Neuro Endocrinol Lett 2007; 28: 477–83. 8. Klimas NG, Salvato FR, Morgan R, Fletcher MA. Immunologic abnormalities in chronic fatigue syndrome. J Clin Microbiol 1990; 28: 1403–10. 62. Snell CF, VanNess JM, Stayer DF, Stevens SR. Exercise capacity and immune function in male and female patients with chronic fatigue syndrome (CFS). In Vivo 2005; 19: 387–90. 92. Brenu EW, Staines DR, Baskurt OK et al. Immune and haemorheological changes in chronic fatigue syndrome. J Transl Med 2010; 8: 1. 93. Klimas NG, Koneru AO. Chronic fatigue syndrome: inflammation, immune function, and neuroendocrine interactions. Curr Rheumatol Rep 2007; 9: 483–7. 94. Fletcher MA, Zeng XR, Barnes Z, Levis S, Klimas NG. Plasma cytokines in women with chronic fatigue syndrome. J Transl Med 2009; 7: 96. 95. Cameron B, Hirschberg DL, Rosenberg-Hassan Y, Ablashi D, Lloyd AR. Serum cytokine levels in postinfective fatigue syndrome. Clin Infect Dis 2010; 50: 278–9. 96. Carlo-Stella N, Badulli C, De Sivestri A et al. The first study of cytokine genomic polymorphisms in CFS: positive association of TNF857 and IFNgamma 874 rare alleles. Clin Exp Rheumatol 2006; 24: 179–82. 97. De Meirleir K, Bisbal C, Campine I et al. A 37 kDa 2-5A binding protein as a potential biochemical marker for chronic fatigue syndrome. Am J Med 2000; 108: 99–105. 98. Sudolnik RJ, Peterson DL, O’Brien K et al. Biochemical evidence for a novel low molecular weight 2-5A-dependent RNase L in chronic fatigue syndrome. J Interferon Cytokine Res 1997;17: Invest in ME (Charity Nr. 1114035) 99. Nijs J, Fremont M. Intracellular immune dysfunction in myalgic encephalomyelitis ⁄chronic fatigue syndrome: state of the art and therapeutic implications. Expert Opin Ther Targets 2008; 12: 281–9. 100. Nijs J, De Meirleir K, Meeus M, McGregor Nr, Englebienne P. Chronic fatigue syndrome: intracellular immune deregulations as a possible aetiology for abnormal exercise response. Med Hypotheses 2004; 62: 759–65. 2011 “(ME)CFS is a disease of unknown aetiology. Major (ME)CFS symptom relief during cancer chemotherapy in a patient with synchronous (ME)CFS and lymphoma spurred a pilot study of Blymphocyte depletion using the anti-CD20 antibody Rituximab, which demonstrated significant clinical response. The…response…suggests that (ME)CFS is an autoimmune disease….The results support the assumption that (ME)CFS is not primarily a mental health disease….The B cells have multiple immune functions, the main ones being antibody production, antigen presentation and regulation of the function and activity of other immune cells, i.e. T-regulatory cells, NK cells and macrophages….We believe the results are best compatible with an autoimmune disease mechanism and that the presented findings may have a major impact on the direction of biomedical research in (ME)CFS” (Oystein Fluge, Olav Mella et al. PloS one: October 2011:6:10:e26358: doi:10.1371/journal.pone.0026358). Replying on 31st October 2011 to criticisms levelled by van der Meer et al, Dr Fluge pointed out that “an autoimmune component is probable in many patients (with ME/CFS)…(and that) (ME)CFS according to Fukuda or Canadian criteria is in many patients a very serious and debilitating disease”. Commenting on the Norwegian study, Dr Gordon Broderick (Associate Professor, University of Alberta) said: “As mentioned by the authors, Rituximab is a B-cell suppressor used in the www.investinme.org Page 95 of 108
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