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

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.
57:03 And there is a colleague of mine, Derya Unutmaz at Jackson Labs, who has found a specific subtype of individuals who have a polarization in their lymphocyte profiles by [inaudible - FACS?] suggesting a prior exposure to viruses. So we are now, we've now extracted those, we've got very good [inaudible - RIN?] numbers, up around 9 and we're in the process of trying to figure out what they've seen, because they're going to be studied using this whole proteome chip.
Click to expand...
 
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
Our Specific Aims are:
1) To determine the frequencies of immune cell subsets in the blood of a clinically defined ME/CFS patient cohort;
2) To assess functional capacity of memory T cells, innate cells and the differentiation potential of naive T cells during ME/CFS; and
3) To determine the T cell and innate cell subset–specific gene and lncRNA transcripts in ME/CFS patient blood samples.
Click to expand...

Our goal is to develop a detailed functional and genetic immunological framework that can be used to
i) decode the mechanisms of ME/CFS and
ii) to develop robust, quantitative immune-biomarker sets for predicting disease susceptibility, stratifying patients and guiding treatment strategies.
Click to expand...
 
Jaybee00 said:
@Jonathan Edwards

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

Thanks
Click to expand...

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.
 
Jonathan Edwards said:
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.
Click to expand...

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).
 
Last edited:
butter. said:
These findings seem a bit weird to me, these are the kind of things we would have found 20 years ago, no?
Click to expand...

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.
 
You must log in or register to reply here.
Back
Top Bottom