Autoantibody targeting therapies in post COVID syndrome and myalgic encephalomyelitis/chronic fatigue syndrome, 2025, Wohlrab et al

Sasha said:
Is it dangerous? It doesn't sound like a very attractive treatment to be on the receiving end of.
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Apheresis can have serious unwanted effects. Shifts in fluid and blood clotting (more or less of it) can produce lethal effects. Like all these things it has got safer with familiarity and people being treated being generally fitter, but it is not free of dangers.
 
Jonathan Edwards said:
I might just throw in that the hint of benefit with all these antibody depleting approaches might be real and masked by suboptimal drug efficacy. (Although it might be a mirage.) But it might not be targeting autoantibody. The benefit might come from depleting perfectly normal antibody!

I will explain more in due course.
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That's interesting. From the Dr Bhupesh Prusty pre-print paper.
Increased circulating fibronectin, depletion of natural IgM and heightened EBV, HSV-1 reactivation in ME/CFS and long COVID, 2023, Liu, Prusty et al
Our data show altered active immune complexes, immunoglobulin-mediated mitochondrial fragmentation as well as adaptive IgM production in ME/CFS patients."
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I wonder if the "Something in the Blood" study by Dr Audrey Ryback and @chillier are perhaps thinking thinking along the lines of Prusty's findings ..... can't wait until they report on their serum/muscle cell study..
 
Jonathan Edwards said:
I think IgG last about 100 days but it varies with antibody and in some cases may be much shorter. That probably means that IgG will recover within a month or two. That is roughly what we saw when patients on rituximab had drops in total IgG levels
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If IgG only lasts 100 days, how would lowering it cause the sort of long term remissions that were reported in the cyclo trial?

Hypothetically speaking.
 
V.R.T. said:
If IgG only lasts 100 days, how would lowering it cause the sort of long term remissions that were reported in the cyclo trial?
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That is a tricky question. Cyclophosphamide was shown to be effective in rheumatoid arthritis but even with big doses the effect wore off completely by 3 months unless you repeated treatment.

The trouble with cyclophosphamide is that it has big effects on T cells as well (and other cells) so if it produces benefit we aren't much the wiser as to what the problem is.
 
Jonathan Edwards said:
That is a tricky question. Cyclophosphamide was shown to be effective in rheumatoid arthritis but even with big doses the effect wore off completely by 3 months unless you repeated treatment.

The trouble with cyclophosphamide is that it has big effects on T cells as well (and other cells) so if it produces benefit we aren't much the wiser as to what the problem is.
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Does Daratumumab also affect T cells etc? Or if that has a positive effect can we narrow down what is potentially being affected?
 
Jonathan Edwards said:
I might just throw in that the hint of benefit with all these antibody depleting approaches might be real and masked by suboptimal drug efficacy. (Although it might be a mirage.) But it might not be targeting autoantibody. The benefit might come from depleting perfectly normal antibody!

I will explain more in due course.
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Verry curious about your hypothesis. Please enlighten us :)

- are you referring to a downstream effect on T-cells?
- and/or the effect of antibodies depletion on the signaling of these antibodies?
 
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