Journal of IiME Volume 6 Issue 1 (June 2012) (ME)CFS patients have autoantibody responses which target epitope or epitopes in the Nterminal region of lamin B1” (Conference Proceedings page 26). Drs Aristo Vojdani, Charles Lapp et al noted that “A prominent feature of (ME)CFS is a disordered immune system. Recent evidence indicates that induction of apoptosis might be mediated in a dysregulated immune system by the upregulation of growth inhibitory cytokines….Increased apoptotic cell population was observed in (ME)CFS individual as compared to healthy controls” (Conference Proceedings page 27). S. Wagner, N Klimas et al: “The purpose of this study was to investigate the relationship between immunologic status and physical symptoms in (ME)CFS patients. The findings suggest that the degree of cellular immune activation is associated with the severity of (ME)CFS physical symptoms. Specifically, elevations in the T-helper/inducer cells, activated T-cells, activated cytotoxic/suppressor T-cells, and CD4/CD8 ratio are associated with greater disease severity”. The immune system abnormalities were (i) a low percentage of cytotoxic T cells; (ii) a low number of cytotoxic T cells; (iii) a high percentage of T helper cells; (iv) a high number of T helper cells; (v) a high CD4/CD8 ratio; (vi) a high number of activated T cells; (vii) a high percentage of cytotoxic T cells; (viii) high numbers of activated T cells (Conference Proceedings page 28). Professor Klimas said that the most important thing in this type of research is to carefully define the study population, and that the lack of definitional rigour may be the reason why study results have conflicted so widely. She also talked about four possible causes of persistent immune activation: (i) a persistent virus, bacteria or toxin; (ii) autoimmune disease; (iii) a ‘super-antigen’ which turns on the entire immune system (e.g. silicone), and (iv) allergy. She recommended that because the immune, endocrine and neurological systems are Invest in ME (Charity Nr. 1114035) interdependent, scientists integrate their findings in (ME)CFS. 1999 On 23rd and 24th April 1999, a “Fatigue 2000” International Conference was held in London. There were 25 speakers, including several from the US as well as from Europe. Many aspects of ME/CFS were addressed, including the immunological dysfunction. Professor Jonathan Brostoff (an immunologist and Director of the Centre for Allergy Research, University College, London) described the type of patient he saw at his clinics and discussed allergy in (ME)CFS. He was emphatic that environmental factors played a much more crucial role in (ME)CFS than has been acknowledged. 1999 “It is of great importance to develop biomarker(s) for differentiation between virally induced (ME)CFS (without sensitivity to chemicals) versus chemically-induced (ME)CFS. Since interferon induced proteins 2-5A Synthetase and Protein Kinase RNA (PKR) have been implicated in the viral induction of (ME)CFS, the objective of this study was to utilise 2-5A and PKR activity for differentiation between (ME)CFS induced by either viruses or chemicals. A clear induction of 2-5A and PKR was observed when MDBK cells were exposed to HHV6, MTBE, and benzene. We conclude that 2-5A and PKR are not only biomarkers for viral induction, but biomarkers to other stressors that include (chemicals)” (Vojdani A, Lapp CW. Immunopharmacol Immunotoxicol 1999:21(2):175-202). 1999 An article from researchers at the Institute of Immunology in Moscow discussed immunity impairment as a result of neurohormonal disorders and noted that at the base of (ME)CFS lie disturbances of the central nervous system, the endocrine system and the immune system: “It was found back in 1987/8 that there is an increase in the level of HLA DR and IL-2 receptors and an increase in the ratio CD4/CD8 in patients www.investinme.org Page 56 of 108
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