Have these so called scientist never seen the many studies showing nk cell dysfunction which is the most common abnormality in cfs/me. NK cells kill viral infections and cancer cells. Do they just not want to belief this science, it seems pretty obvious why cfs/me patients dont feel well.
Heres a few for them to read: There are a surprisingly large number of human natural killer (NK) cell deficiency states that provide insight into the role of NK cells in defense against human infectious disease. Many disorders associated with NK cell defects are caused by single gene mutations and, thus, give additional understanding concerning the function of specific molecules in NK cell development and activities. A resounding theme of NK cell deficiencies is susceptibility to herpesviruses, suggesting that unexplained severe herpesviral infection should raise the possibility of an NK cell deficit.
http://www.ncbi.nlm.nih.gov/pubmed/12505527
Results: Compared to healthy individuals, CFS/ME patients displayed significant increases in IL-10, IFN-g, TNF-a,
CD4+CD25+ T cells, FoxP3 and VPACR2 expression. Cytotoxic activity of NK and CD8+T cells and NK phenotypes, in
particular the CD56bright NK cells were significantly decreased in CFS/ME patients. Additionally granzyme A and
granzyme K expression were reduced while expression levels of perforin were significantly increased in the CFS/ME
population relative to the control population. These data suggest significant dysregulation of the immune system
in CFS/ME patients.
Conclusions: Our study found immunological abnormalities which may serve as biomarkers in CFS/ME patients
with potential for an application as a diagnostic tool.
http://www.translational-medicine.com/content/pdf/1479-5876-9-81.pdf
Chronic fatigue syndrome (CFS) is a specific clinical condition that characterises unexplained disabling fatigue and a combination of non-specific accompanying symptoms for at least 6 months, in the absence of a medical diagnosis that would otherwise explain the clinical presentation. Other common symptoms include headaches, myalgia, arthralgia, and post-exertional malaise; cognitive difficulties, with impaired memory and concentration; unrefreshing sleep; and mood changes. Similar disorders have been described for at least two centuries and have been differently named neurasthenia, post-viral fatigue, myalgic encephalomyelitis and chronic mononucleosis. Recent longitudinal studies suggest that some people affected by chronic fatigue syndrome improve with time but that most remain functionally impaired for several years. The estimated worldwide prevalence of CFS is 0.4-1% and it affects over 800,000 people in the United States and approximately 240,000 patients in the UK. No physical examination signs are specific to CFS and no diagnostic tests identify this syndrome. The pathophysiological mechanism of CFS is unclear. The main hypotheses include altered central nervous system functioning resulting from an abnormal immune response against a common antigen; a neuroendocrine disturbance; cognitive impairment caused by response to infection or other stimuli in sentient people. The current concept is that CFS pathogenesis is a multifactorial condition. Various studies have sought evidence for a disturbance in immunity in people with CFS. An alteration in cytokine profile, a decreased function of natural killer (NK) cells, a presence of autoantibodies and a reduced responses of T cells to mitogens and other specific antigens have been reported. The observed high level of pro-inflammatory cytokines may explain some of the manifestations such as fatigue and flu-like symptoms and influence NK activity. Abnormal activation of the T lymphocyte subsets and a decrease in antibody-dependent cell-mediated cytotoxicity have been described. An increased number of CD8+ cytotoxic T lymphocytes and CD38 and HLA-DR activation markers have been reported, and a decrease in CD11b expression associated with an increased expression of CD28+ T subsets has been observed. This review discusses the immunological aspects of CFS and offers an immunological hypothesis for the disease processes.
http://www.ncbi.nlm.nih.gov/pubmed/18801465
INTRODUCTION
NK cell deficiency syndromes are rare disorders in which NK cells are absent, deficient, or dysfunctional, in the absence of any other identifiable immunodeficiency, genetic disorder, or medication known to affect NK cells.
The management of patients with these disorders is discussed here. The biology of NK cells, the clinical manifestations of NK cell disorders, and the evaluation of patients suspected of having NK cell defects are presented separately. (See "NK cell deficiency syndromes: Clinical manifestations and diagnosis".)
OVERVIEW
Therapy for patients with NK cell deficiency syndromes is largely empiric, due to the small numbers of cases described in the literature. Active infections must be identified and treated aggressively, as with any immune disorder. The use of specific therapies is based either on theoretical utility or anecdotal reports of benefit (table 1).
ANTIVIRAL PROPHYLAXIS
NK cell disorders are characterized clinically by susceptibility to severe and/or recurrent infection with herpes viruses, including varicella zoster virus (VZV), Herpes simplex virus (HSV) I and II, Epstein Barr virus (EBV), and cytomegalovirus (CMV). There is also a marked susceptibility in some patients to Human Papilloma Viruses.
Prophylactic antiviral regimens should be tailored to the infectious history of the individual patient. Serologic tests should be performed to determine if an NK cell deficient individual has experienced infections with known herpesviruses. In our clinic, we assess for past exposure to the following viruses:
http://www.uptodate.com/contents/nk-cell-deficiency-syndromes-treatment
Theres more out there but this should be enough for them to read up on to start with, how easy is it to find this information????
cheers!!!