Journal of IiME Volume 6 Issue 1 (June 2012) suffering from this syndrome” (Artsimovich NG et al. Russ J Immunol 1999:4(4):343-345). It is notable that Russian researchers were aware of these cardinal biomarkers of (ME)CFS as long ago as 1999, but that eight years later, the NICE Guideline Development Group who produced the Clinical Guideline on “CFS” (who were clearly influenced by the Wessely School but who were acclaimed by NICE as “experts” in the disorder) were apparently unaware of these diagnostic biomarkers. 1999 The Second World Congress on (ME)CFS and Related Disorders took place on 9th-12th September 1999 in Brussels; as was the First World Congress in 1995, it was organised by Professor Kenny DeMeirleir. Medical experts from around the world presented their most recent findings in 48 oral and 26 poster presentations to an estimated 150 conference delegates. Professor Nancy Klimas gave a comprehensive and authoritative overview entitled “Immunological Abnormalities in CFS”. She started by listing various factors affecting the immune system in (ME)CFS: (i) genetic predisposition (51%); (ii) triggering events (infections), and (iii) mediators (endocrinological and psychological factors), observing that the health outcome in any individual depends on how all these interact. She said the role of the immune system in illness is twofold: (1) it plays a direct role in contributing to the symptom complex: immune competence decides effective or defective prevention of reactivation of infections. When turned on, the lymphocyte antigen-driven response may generate a Type I response (CD4+, Th1, IL 2 / IL 12, INF - gamma, with activation of CD8+ cells that kill viruses). Lymphocytes play a vital role: they function through a messenger system -- cells have memories; they are antigen-driven and recognise infections, transplants, toxins, foods etc. Invest in ME (Charity Nr. 1114035) (2) it plays an indirect role, because it interacts with the brain (it has receptors for neurotransmitters) and with the endocrine system. Cortisol reduces inflammation through down-regulation of immune activation -- low cortisol in CFS could play a role in chronic immune activation. Stress has a profound impact on the immune system. Interaction with the hypothalamic/pituitary axis affects neurotransmitters and impacts on sleep. The Type II response (Th2, IL6, IL10, activation of B cells, and antibody production, which prevents/clears infection) comes to dominate as the illness extends. The importance of the 2-5 RNase -L (a product of INF- gamma activation) leads to an up-regulation of RNA synthesis and pro-inflammatory cytokines, TNF -alpha and IL 1, which also disturb circadian rhythms. Specific oligoclonal and not polyclonal antibodies are involved. With regard to oligoclonal versus polyclonal activation, Professor Klimas observed that there is a lack of abnormal serology to most latent viruses, suggesting that immune activation was antigen-specific. The effects of stress and negative life events were similar in CFS patients and in controls, but the long-term outcome depends on the shift from Th1 to Th2. There is evidence of chronic immune activation: enzyme systems are up-regulated (e.g. interferon, 2-5A RNase L activation, mRNA (cytokines). There is evidence of cytokine abnormalities – cytokines change over time and with illness severity: TNF-alpha receptor expression increases with flares of the illness, and there is increased evidence of Type II expression as the illness persists for years. Long-term, stress results in immune dysfunction illness (e.g. reduced numbers of CD8 (suppressor) cells, blunted growth hormone (GH) response and thyroid releasing factor (TRF), www.investinme.org Page 57 of 108
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