Discussion in 'Latest ME/CFS Research' started by lansbergen, Mar 23, 2013.
I concluded decades ago something was wrong with Tcell function.
Levamisole improves Tcell function.
Very similar finding to bond uni/PHANU in australia
Do you have a link?
Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME) is characterised by severe prolonged
fatigue, and decreases in cognition and other physiological functions, resulting in severe loss of quality of life,
difficult clinical management and high costs to the health care system. To date there is no proven
pathomechanism to satisfactorily explain this disorder. Studies have identified abnormalities in immune function
but these data are inconsistent. We investigated the profile of markers of immune function (including novel
markers) in CFS/ME patients.
We included 95 CFS/ME patients and 50 healthy controls. All participants were assessed on natural killer
(NK) and CD8
+T cell cytotoxic activities, Th1 and Th2 cytokine profile of CD4+T cells, expression of vasoactive
intestinal peptide receptor 2 (VPACR2), levels of NK phenotypes (CD56
bright and CD56dim) and regulatory T cells
expressing FoxP3 transcription factor.
Compared to healthy individuals, CFS/ME patients displayed significant increases in IL-10, IFN-g, TNF-a,
+CD25+ T cells, FoxP3 and VPACR2 expression. Cytotoxic activity of NK and CD8+T cells and NK phenotypes, in
particular the CD56
bright 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.
Our study found immunological abnormalities which may serve as biomarkers in CFS/ME patients
with potential for an application as a diagnostic tool.
I always said part of the immune system fails and another part goes in overdrive to try to compensate for that.
Hmm, makes me wonder that if the success of Rituximab is less attributable to the lack of B-cells post treatment but rather the way T-cells are forced to function in the absence of B-cells.
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