Perturbation of effector and regulatory T cell subsets in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) (2019) Karhan, Unutmaz et al

https://twitter.com/user/status/1208052662870122498


Moderator note: See this post in the thread for the preprint.

 

So maybe there might be some benefit to wiping out abnormal T cells with cyclophosphamide.....

 

Lipkin is already looking at these subsets. The collaboration is really good to see, happening before publication! This is a quote from the end of Ian Lipkin's CDC talk taken from the YouTube transcript.

 

These guys are also going to publish soon. Hopefully these in-depth investigations will finally reveal something about the cause of the illness.

https://twitter.com/user/status/1208085323550482437

 

For those that don't know, Brodin Petter is from the Karolinska Institute in Sweden.

 

Let's see the proper data, but it would be interesting if it holds up.

If we want to knock out T cells Campath-1H is that thing to use.

 

I'm assuming this is the project that was started 1 June 2016, before the centers were announced, and funded at $650,000 per year per this information. No ME/CFS papers have been reported under this grant yet.

Title : DECODING IMMUNOLOGICAL PERTURBATIONS DURING CHRONIC FATIGUE SYNDROME
https://projectreporter.nih.gov/project_info_description.cfm?aid=9716375&icde=31258613

 

@Jonathan Edwards

Campath-1H is less dangerous in your opinion than cyclophosphamide? Also what is the difference between Campath-1H (humanized) and Alemtuzumab?

Thanks

 

I think alemtuzumab is the post-hoc generic name for the same antibody that started out as Campath. It targets CD52 which is on all lymphocytes but the long term effect is restricted to memory T cells since B cells return after about 3 months.

T cell depletion with a monoclonal is much better in terms of benefit/side effects. Enough cyclo to deplete T cells long term means violent nausea and infection risk from neutropenia. Smaller doses of cyclo have little long term effect.

 

These findings seem a bit weird to me, these are the kind of things we would have found 20 years ago, no?

I also remember Dr. Davis saying that when he lowered Th17, some markers actually got worse (gut permeability).

 

Not sure what you are referring to exactly. So far we have not been told what the findings are. MAIT cells did not exist 20 years ago. But it is true that several other groups have looked at lymphocyte subsets and not found anything very dramatic.

 

That raises all sorts of interesting epistemological questions.

 

No it just means I was teasing.

 

A short while ago we had a thread in which strong views were expressed regarding the use of sarcasm and irony.

 

Long ago i got the finding that "Approximately 33 % of the CD4+ T-lymphocytes are CD45RA and CDRO double positive", always been curious if it had any relevance to ME. Wonder if they looked at that

 

Checked the price, and assume this to be way out of any ME-research funding league... Are there any cheaper options that could work?

 

I do not want to.

 

If there was good evidence for it being a sensible thing to use the cost would not be a big issue. It is similar to rituxmab and we have already had a full size phase 3 trial of that.

 

In no universe its the same cost as Rituximab lol haha. One dose of Rituximab 500mg is around 2000€ and it last for 3-6 months. One dose of Lemtrada cost 20000€ and it last for 3 days.

https://multiplesclerosis.net/living-with-ms/lemtrada-economics-ms-treatments/

 

If you have low amounts of T regulatory cells do you then get high levels of activated T cells I wonder with my crude understanding of this