Not sure why Peter White is interested in cytokines. Mary Fletcher, I believe it was, said that many studies don't use to date techniques but that their lab consistently finds cytokine issues in ME/CFS.
That said it's true there's very little consistency in the literature. Cytokine levels may not matter much of even small increases in cytokines are enough to set off the microglia. Plus Broderick believes that even normal levels of some cytokines can set off a bizarre reaction if the immune network itself is tweaked. Younger on the other hand, used networking analysis I think it was to identify leptin as the key driver of symptoms in the good day/bad day study...I believe it was only mildly elevated otherwise.
It's a very complex subject with new ways emerging how to analyse it.
Exercise has been associated with C4a (complement) increases in the blood or in gene expression in two studies. That apparently didn't make the paper.
TBG-B, however - the one cytokine that was consistently abnormal - could be important. The paper said"
The observations therefore seem to be consistent with a biologically significant elevation in the cytokine concentration in CFS. The clinical significance of a raised TGF-β is unclear in CFS, but its associations with clinical symptoms, severity and prognosis merits further evaluation.
As an immune mediator, TGF-β has both pro- and anti-inflammatory effects. The intracellular signal transduction, following engagement of the TGF-β receptor, depends upon the cell type and context in which the cell is activated.
TGF-β's inhibitory effect on activated leukocytes means it could be turning the immune system down. It may be attempting to turn off activated microglia; that is increased TGF-B may be a sign of neuroinflammation. TGF-β is also associated with alterations in cerebral blood flow (Gaertner et al., 2005). It also appears to depress motor activity and it's associated with increased free radical production during exercise. It's an interesting cytokine...
That said it's true there's very little consistency in the literature. Cytokine levels may not matter much of even small increases in cytokines are enough to set off the microglia. Plus Broderick believes that even normal levels of some cytokines can set off a bizarre reaction if the immune network itself is tweaked. Younger on the other hand, used networking analysis I think it was to identify leptin as the key driver of symptoms in the good day/bad day study...I believe it was only mildly elevated otherwise.
It's a very complex subject with new ways emerging how to analyse it.
Exercise has been associated with C4a (complement) increases in the blood or in gene expression in two studies. That apparently didn't make the paper.
TBG-B, however - the one cytokine that was consistently abnormal - could be important. The paper said"
The observations therefore seem to be consistent with a biologically significant elevation in the cytokine concentration in CFS. The clinical significance of a raised TGF-β is unclear in CFS, but its associations with clinical symptoms, severity and prognosis merits further evaluation.
As an immune mediator, TGF-β has both pro- and anti-inflammatory effects. The intracellular signal transduction, following engagement of the TGF-β receptor, depends upon the cell type and context in which the cell is activated.
TGF-β's inhibitory effect on activated leukocytes means it could be turning the immune system down. It may be attempting to turn off activated microglia; that is increased TGF-B may be a sign of neuroinflammation. TGF-β is also associated with alterations in cerebral blood flow (Gaertner et al., 2005). It also appears to depress motor activity and it's associated with increased free radical production during exercise. It's an interesting cytokine...
![ME/CFS lecture | Dr Nancy Klimas | 2011 [Chronic Fatigue Syndrome / SEID / New Zealand] - YouTube](data:image/gif;base64,R0lGODlhAQABAIAAAAAAAP///yH5BAEAAAAALAAAAAABAAEAAAIBRAA7)
