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I sort of see your point but when I was moderate I could mostly manage by myself around thr house and now I am severe I need care with so many things every day and struggle to put together a basic snack in the kitchen while sitting on an office chair. Also I feel like we do need to know if...

I think with the exponential level of disability increase with MECFS severity, everybody feels they have a lot to lose. As a severe pwME who has experienced very severe I know I do.

Surely when you do a drug trial its best to start with people who are the most afflicted by a disease? I understand excluding very severe because of their extreme vulnerability, and why F&M now exclude mild cos of fluctuation, but I think excluding severe would be a mistake personally.

Is it concievable that if there is a gdT cell pathology, Campath might not be effective but the gdT monoclonal might? Or a similar situation for any specific T cell subset? Or is it the case that if Campath doesn't work all those hypotheses are bust?

Are there any physician researchers in the ME/CFS field now who could conceivably take a trial like this on?

This is a good point, although I would argue that depending on what the ADE is it might be the same for both.

Is there any link between CRH, especially in hypothalamus and gamma delta T cells or BTN2A1/2A2 generally?

I think focusing on severe/very severe here is a good idea. What are the implications that potential trial participants should understand? And if we are focussing on severe and very severe, can campath be administered in a home setting?

I asked this question in the BTN2A1/2 thread but don't want to keep clogging that thread up. So ill quote some of the things I said there here: In a manner analogous to ritux/dara for a general and specific approach to B cells and then LLPCs, perhaps there could be a pilot looking at...

https://www.science.org/doi/10.1126/sciimmunol.aeg4759 Also, this paper posted in misc research looks relevant to this post but I cant read it. Although the post was discussing BTN2A2 not 1. I'm not sure if BTN2A1 has the same links to FOXP3 and Tregs

Isn't this stuff prohibiviely expensive? Is it conceivable that it will become affordable enough to be standard?

Again, the gdT conundrum and the broader T cell hypothesis all seems quite similar to the B cell/autoantibody situation, where there are a lot of theories and a lot of things that you'd expect to see that we don't, and a lot of possibilities that would be hard to prove through the basic science...

The fact that these are involved in CNS autoimmunity is an interesting connection

In that case, maybe there is an argument for getting a good quality pilot or small phase 2 (if drug already approved) study set up now.

I was talking generally in that post.

Iirc cyclo had a positive phase 2 and responders were better years after follow up. They didnt go ahead with phase 3 because of how toxic it is and pivoted to dara.

Are there any physician researchers who would have experience giving T cell drugs in the way Fluge and Mella have for B cell drugs?

https://na.eventscloud.com/website/70485/home/ A quick google threw up this 2025 meeting of a biannual gdT conference. Maybe its worth contacting the key note speakers Erin Adams (Chicago) https://na.eventscloud.com/ereg/popups/custompopup.php?popupid=161780 Bruno Silva Santos (IMM Lisbon)...

Absolutely! There does seem to be a lot of evidence and hypothesising possibly implicating various kinds of T cells and yet we've had no T cell clinical trials, and a good few B cell/antibody ones, and I'm not sure the evidence for B cells is any stronger than T cells.

Is anyone looking into the possible role of specifically gamma delta T cells in MECFS? could we get some gdT cell experts interested based on DecodeME if not?