Journal of IiME Volume 6 Issue 1 (June 2012) Professor Komaroff said that researchers have become more interested in the immunological abnormalities, and among the more consistent findings are depressed activity of NK cells and increased number of certain T-cell. Recent studies have found unusual antibodies attacking the nucleus of cells in (ME)CFIDS patients: “These have not been seen with this frequency in other illnesses”. Professor Klimas said that a temptation for doctors pondering how to approach treatment for (ME)CFIDS patients is to look at the activated immune system and try to calm it down, but “the dilemma in (ME)CFS is that we don’t know why that activity is there. We don’t know if this activation is in response to something in the body that needs the immune system to protect it. You run the risk of suppressing the immune system so I don’t think that’s a fair target now for (ME)CFS treatment” (The CFIDS Chronicle, January/February 1998). 1998 On 11th – 13th February 1998 a conference entitled “The Clinical and Scientific Basis of Chronic Fatigue Syndrome: From Myth towards Management” was held at Manly, Sydney, at which notable speakers included Dr David Bell, Dr Peter Rowe, Dr Martin Lerner, Dr Charles Lapp, Dr Byron Hyde, Dr Hugh Dunstan, Dr Neil McGregor, Dr Richard Burnet, Professor Gary Scroop and Professor Kenny De Meirleir. Speakers noted the detection of abnormalities in immunological measures including the CD4:CD8 ratio, an abnormality in NK cells and positive anti-nuclear antibodies. Colin Little presented a paper on the relationship of TGF and its relationship to fatigue and food intolerance, explaining that if small amounts of an ingested antigen (i.e. food) induce TGF and Th2 cells (which produce IL-4 and IL-10), then active suppression of protective Th1 cells occurs, with the result that patients experience intolerance/allergies to food, accompanied by autonomic symptoms. 1998 On 16th July 1998 Professor Stephen Straus from the USA gave a lecture at the Royal College of Invest in ME (Charity Nr. 1114035) Physicians, London, in which he said: “It is a disease that perhaps arises from immune dysfunction….There are reasons to implicate immune problems in CFS…There are many published reports of a range of immune abnormalities – immunoglobulin deficiencies, increased levels of cytokines, abnormal T cell subsets and NK cells”. 1998 “The increased expression of Class II antigens and the reduced expression of the co-stimulatory receptor CD28 lend further support to the concept of immunoactivation of T-lymphocytes in (ME)CFS and may be consistent with a viral aetiopathogenesis in the illness. We report, for the first time, increased expression of the apoptosis repressor protein bcl-2 (and) we demonstrated changes in different immunological parameters, each of which correlated with particular aspects of disease symptomatology (and) measures of disease severity” (IS Hassan, WRC Weir et al. Clin Immunol & Immunopathol 1998:87:1:60-67). 1998 The fourth Biennial AACFS International Research and Clinical Conference was held on 10th – 12th October 1998 at Cambridge, Massachusetts, with over 60 doctors and researchers attending. Professors Klimas, Fletcher and Patarca et al described (ME)CFS as “an illness which is associated with immune dysfunction, including abnormalities in the function of lymphocytes and expression of pro-inflammatory cytokines” (Conference Proceedings, page 19). Dr Eng Tan et al (from the Autoimmune Disease Centre and Department of Cell Biology, the Scripps institute, La Jolla, California) noted: “In previous studies (J Clin Invest 1996:98:1888-1896; Arthritis Rheum 1997:40:295-305) it was found that patients with (ME)CFS had autoantibodies to a relatively insoluble cellular antigen localised at the nuclear envelope called lamin B1….(Results) suggested that there might be an epitope on lamin B1 that was specific for (ME)CFS…..Conclusion: www.investinme.org Page 55 of 108
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