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Harriet Hall CFS: Rituximab Revisited in Science-Based Medicine

msf

Senior Member
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3,650
So...is it possible? Would a reduction of cytokine levels be expected to be occur through any of those potential mechanisms?
 

msf

Senior Member
Messages
3,650
I guess that ´T-cell polarization to a suppressive phenotype´ would cause cytokine reduction. When I thought about it, I realised that autoinflammatory diseases probably involve inflammatory cytokines - could this be how Ritux works in RA?
 
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do you know any more details about the german group ? like is there anywhere I could read about the dosage and frequency etc ?
regarding subgroups, I do not in any way mean to be disrespectful or dismissive but why would we think that autoimmune/immune dysfunction driven CFS people are a slice as opposed to all of us when we are talking about people who fit the more robust criteria (PEM , memory problems, comprehension and word finding problems, unrefreshing sleep, sensory overload, POTS or less specific OI etc) ? If NK cells being both ineffective and low in number is a common characteristic wouldn't this indicate most of us are this way either because of or VIA a mechanism of a now errant immune system ?
I ask because I want to keep my own expectations firmly in check RE this medication but at the same time I imagined that ritux or related drugs would easily treat more than 20% of us. don't we still have a long way to go with observing the rate and effect of B-cell depletion so a balance can be struck with spacing between infusions, how long a treatment schedule goes for and the actual dosage ?
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Marky90

Science breeds knowledge, opinion breeds ignorance
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1,253
I think Jonathan would have to answer that..

But both B-cells and T-cells can produce cytokines, so for me it seems to be in the realm of possibility:p
Also, endothelial cells can produce it. So if an proposed autoimmune attack against those cells seizes? Who knows, not me..