Journal of IiME Volume 6 Issue 1 (June 2012) disease “tell us this is an autoimmune response to something”; autoimmune-like parameters included “enhanced T4 helper cell numbers (and) decrease in T8 cells, which is a model in the MRL mouse for autoimmunity”. At that Conference, Drs Anthony Komaroff and Paul Cheney outlined some of the laboratory findings in people with CFIDS; these include lymphocytosis; low level ANA; monocytosis; antithyroid antibodies; elevated transaminases; circulating immune complexes; elevated B cell numbers; depressed levels of IgA; elevated T4/T8 ratio; NK cells not stimulated by IL-2, and elevated levels of cytokines – including IL-2 levels 50 times higher than normal (The CFIDS Chronicle, Spring 1989). Dr Paul Cheney noted that 70% of ME/CFS patients tested had depressed levels of salivary IgA (SIgA), and that ME/CFS patients with low SIgA levels tended to have high levels of insoluble circulating immune complexes. Microscopic analysis of tissues showed lymphocytic vasculitis (lymphoid infiltrates in the blood vessel wall) in 75% of patients tested. Reporting this medical conference, (Meeting Place issue 32), the Journal of the Australia and New Zealand ME Society (ANZMES) stated in its December 1989 issue: “The consensus of the conference was that CFIDS represents a growing pandemic of immune dysfunction”. 1989 The Summer/Autumn (Fall) 1989 issue of The CFIDS Chronicle was a 180 page journal that reported on numerous conferences on (ME)CFS at which the immunological abnormalities were confirmed; it also addressed other areas of medical research into the disorder. One book in particular was reviewed, this being “The Body at War: The Miracle of the Immune System” by Professor John M Dwyer (New York NAL Books, 1988; 253 pages). The CFIDS Chronicle reviewer (Dr Dennis Jackson) noted that Dwyer, an Australian immunologist, condemned the Invest in ME (Charity Nr. 1114035) “intellectual arrogance” of his fellow physicians who have continued to chase easy theories about the psychiatric origin of the disorder and that Dwyer declared: “Unfortunately, continued widespread ignorance of the condition perpetuates psychological harassment for many….A genetic defect downgrading the efficacy of a response to infection should translate into an immunological defect, and this has now been established as fact. The reproducible demonstration of T-cell abnormalities in patients with (ME)CFS is the reason we are discussing this disease in this book on the immune system….Patients with classical symptoms of (ME)CFS almost always have reduced numbers of immunoregulatory cells in their blood….So consistent are these abnormalities they allow us to make a positive diagnosis”. 1989 “Our investigations suggest that (ME)CFS is characterized by objective laboratory abnormalities. A more appropriate name for this syndrome would be chronic fatigue-immune dysfunction syndrome (CFIDS), since immune dysfunction appears to be the hallmark of the disease process” (Nancy Eby , Seymour Grufferman et al. In: Natural Killer Cells and Host Defense. Ed: Ades EW and Lopez C. 5th International Natural Killer Cell Workshop. Pub: Karger, Basel, 1989:141-145). 1989 “(ME)CFS has been associated with abnormal T cell function. These patients have diminished phytohaemagglutinin-induced lymphocyte transformation and decreased synthesis of interleukin. We studied the display of CD3, CD5, CD2, CD4, CD8 and Leu-M3-defined antigen in peripheral blood mononuclear cells in (ME)CFS who fulfilled the (1988 Holmes et al) criteria. Patients had reduced expression of CD3. These data indicate that in (ME)CFS, some patients have T lymphocytes (CD2- and CD5- positive cells) without immunoreactive CD3” (ML Subira et al. The Journal of Infectious Disease 1989:160:1:165166). www.investinme.org Page 36 of 108
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