Journal of IiME Volume 6 Issue 1 (June 2012) Il-6, IL-10 and IL-12 are of research interest NK cell function should be measured as soon as possible following blood draw, within 4 hours Researchers should consider the effect of the endocrine system on the immune system A chronic infection may be causing the immune activation seen in (ME)CFS patients. 1997 On 17th January 1997 Dr Darryl See (Head of the CFIDS Clinic at the University of California, Irvine) gave a lecture in Los Angeles entitled “New Concepts in Cause and Treatment of CFIDS”, noting the low levels of IgG3 and IgG1 and the consequent loss of anti-viral activity, and the very, very low levels of IL-10 in people with (ME)CFIDS, pointing out that IL-10 is a down-regulator of the immune system and in normal people calms it down by decreasing the number of inflammatory cytokines. He also warned about taking prednisone: “You only take prednisone if you’re in the T-cell activation group. If you have natural killer cell dysfunction, and you give a lot of prednisone, your NK cell activity will go down (further) and you’ll start reactivating viruses. dangerous”. It’s 1997 Dr Charles Shepherd from the UK ME Association published an article in the British Journal of Social Work (1997:27:755-760) in which he drew attention to the most relevant findings to date, including the immunological dysfunction in ME/CFS: “Almost all reported studies have found laboratory abnormalities”, citing Strober W (1994) “Immunological function in chronic fatigue syndrome”; in: Straus S (ed): Chronic Fatigue Syndrome; New York, Mark Dekker, pp 237-240. 1997 “The level of bioactive transforming growth factor was measured in serum from patients with (ME)CFS and compared with normal controls, patients with major depression, patients with Invest in ME (Charity Nr. 1114035) systemic lupus erythematosus and patients with multiple sclerosis. Patients with (ME)CFS had significantly higher levels of bioactive TGF than the healthy controls, patients with major depression, patients with systemic lupus erythematosus and patients with multiple sclerosis. Of greatest relevance to (ME)CFS are the effects of TGF on cells of the immune and central nervous systems. There is accumulating evidence that TGF may play a role in autoimmune and inflammatory diseases” (AL Bennet, AL Komaroff et al. J Clin Virol 1997:17:2:160-166). 1997 “(ME)CFS is associated with dysregulation of both humoral and cellular immunity, including mitogen response, reactivation of viruses, abnormal cytokine production, diminished natural killer (NK) cell function, and changes in intermediary metabolites. The biochemical and immunologic data presented here identified a subgroup of individuals with (ME)CFS with an RNase L enzyme dysfunction that is more profound than previously observed (and) is consistent with the possibility that the absence of the 80-kDa and 40-kDa RNase L and presence of the LMW RNase L correlate with the severity of (ME)CFS clinical presentation” (Robert Suhadolnik, Daniel Peterson, Paul Cheney et al. Journal of Interferon and Cytokine Research 1997:17:377-385). Professor Suhadolnik explained in lay terms the significance of this paper (reported by Patti Schmidt in CFIDS Chronicle, Summer 1997, page 17): “He has found a particular place in the immune system, the 2-5 RNase L antiviral pathway, where something is wrong. ‘The whole antiviral pathway heats up out of control’ explained Suhadolnik. ‘You’re really sick physiologically. Your body just keeps going and going like the Energiser bunny, making ATP and breaking it down. No wonder you’re tired’. He’s found a novel protein in CFIDS patients in that viral pathway. ‘In most cases, the human body is able to resist infection thanks to a cascade of biochemical events triggered by the body’s immune system. If these antiviral defence pathways are functioning correctly, the spread of the virus is prevented’. www.investinme.org Page 53 of 108
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