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(Video) OMF Scientific Advisory Board Member Mark Davis, PhD, Presents An Update on ME/CFS Research

Ben H

OMF Volunteer Correspondent
Messages
1,131
Location
U.K.
OMF%20End%20MECFS%20logo%20.jpg

OMF Scientific Advisory Board Member Mark Davis, PhD, Presents
An Update on ME/CFS Research

Dear all,

We are pleased to share a new research update by OMF's Scientific Advisory Board member, Mark M. Davis, PhD, produced by Ashley Haugen for this #OMFScienceWednesday.
Dr. Mark Davis, Director of the Stanford Institute for Immunity, Transplantation, and Infection, talks about his work with T-cells to understand their role in ME/CFS and to determine if ME/CFS is an autoimmune disease. Watch the video here.


To support this important research, please donate now.

With hope for all,

linda%20signature%20001.jpg

Linda Tannenbaum
CEO/President


www.omf.ngo

@Janet Dafoe (Rose49) @AshleyHalcyoneH @marilynbsg
 

Ben H

OMF Volunteer Correspondent
Messages
1,131
Location
U.K.
Just watched the video myself...what a cool dude Mark is. Sounds very exciting..I’d like to see what these candidates are. Love the respect shown towards the whole team, Mark is a mega name in his field.

Big thanks to Ashley for her hard work making the videos and all the editing. She works so hard for the cause.


B
 

ScottTriGuy

Stop the harm. Start the research and treatment.
Messages
1,402
Location
Toronto, Canada
As much I appreciate and support the work of the OMF, it just makes me cringe when he used the term 'chronic fatigue' 3 times in the first 1:40.

Surely he is aware of how the conflation of 'chronic fatigue' and 'chronic fatigue syndrome' (and with the later, the term itself) have, and continue to undermine our collective efforts.

Sigh.
 
Messages
87
As much I appreciate and support the work of the OMF, it just makes me cringe when he used the term 'chronic fatigue' 3 times in the first 1:40.

Surely he is aware of how the conflation of 'chronic fatigue' and 'chronic fatigue syndrome' (and with the later, the term itself) have, and continue to undermine our collective efforts.

Sigh.

I think he and Ron are doing that precisely for this reason, to avoid patients being discriminated because their doctor tells them "you have chronic fatigue not me/cfs so it's psychosomatic". Maybe i'm wrong but it would make sense.
 

Diwi9

Administrator
Messages
1,780
Location
USA
It would be interesting to hear how T-cell clonal expansion and the metabolic trap hypothesis might tie into one another. I have many markers for an increased risk of auto-immune diseases and have family members with them (MS, ulcerative colitis, Hashimoto's)...is anyone aware of survey/study data showing that PwME tend to come from families with histories of auto-immunity?
 

Hopeful1976

Senior Member
Messages
345
I am so appreciative of all of this research - it is truely amazing; but I didn't hear anything different to what was said at the symposium last year? Please correct me if I am wrong...
 

Frenchguy

Senior Member
Messages
119
Location
France
It would be interesting to hear how T-cell clonal expansion and the metabolic trap hypothesis might tie into one another. I have many markers for an increased risk of auto-immune diseases and have family members with them (MS, ulcerative colitis, Hashimoto's)...is anyone aware of survey/study data showing that PwME tend to come from families with histories of auto-immunity?

I think that the "impaired enzyme" mentionned for the metabolic trap hypothesis can have a great effect on the regulatory part of the immune system.
 

neweimear

Senior Member
Messages
215
As much I appreciate and support the work of the OMF, it just makes me cringe when he used the term 'chronic fatigue' 3 times in the first 1:40.

Surely he is aware of how the conflation of 'chronic fatigue' and 'chronic fatigue syndrome' (and with the later, the term itself) have, and continue to undermine our collective efforts.

Sigh.
Oh God, me too. I can't take 'chronic fatigue'. So grateful for all the work but please use ME/CFS.
 

neweimear

Senior Member
Messages
215
I am so appreciative of all of this research - it is truely amazing; but I didn't hear anything different to what was said at the symposium last year? Please correct me if I am wrong...
I thought the same, they are still obviously searching but no answers just yet. We just have to hope that it's sooner rather than later.
 

ljimbo423

Senior Member
Messages
4,705
Location
United States, New Hampshire
I wonder how it fits with the role of the gut causing illnesses because of immune activation.

Hi Pam- This study shows that lipopolysaccharides (LPS) from gram negative bacteria, many of which, live in the gut as a part of the normal microbiome.

Activate CD8+ T cells, which would lead to there cloning. Which is what Mark Davis is talking about in the video.

If someone had increased intestinal permeability, than that would increase the level of LPS in the blood, causing immune activation. Part of that immune activation could be CD8+ T cells.

Direct recognition of LPS by human but not murine CD8+ T cells via TLR4 complex.

Abstract
LPS comprises a major PAMP and is a key target of the immune system during bacterial infection. While LPS can be recognised by innate immune cells via the TLR4 complex, it is unknown whether T lymphocytes, especially CD8(+) T cells are also capable of doing so.

We report here that naive human CD8(+) T cells, after activation by TCR stimulation, express surface TLR4 and CD14. These activated CD8(+) T cells can then secrete high concentrations of IFN-gamma, granzyme and perforin in response to LPS.

These effects can be specifically inhibited using siRNA for TLR4. Furthermore, LPS can synergize with IL-12 to polarize the CD8(+) T cells into cytotoxic T-cell 1 (Tc1) that produce IFN-gamma but not IL-4, with or without TCR activation.

Moreover, CD8(+)CD45RO(+) memory T cells constitutively expressed TLR4 and markedly enhanced IFN-gamma production when stimulated with LPS. In contrast, activated murine CD8(+) T cells lack TLR4 and CD14 expression and fail to respond to LPS for proliferation and cytokine production.

Thus, human but not murine CD8(+) T cells are able to directly recognise bacterial LPS via LPS receptor complex and TLR4 provides a novel signal for the activation of effector and memory human CD8(+) T cells.
LINK

Here is a study that shows LPS activate CD8+ T cells in rheumatoid arthritis.



Jim
 

Sushi

Moderation Resource Albuquerque
Messages
19,934
Location
Albuquerque
Big thanks to Ashley for her hard work making the videos and all the editing. She works so hard for the cause.
I really want to second that and let @AshleyHalcyoneH how much we appreciate these videos. She also has the sensitivity to edit them into a short enough version that most of us can take them in!
It would be interesting to hear how T-cell clonal expansion and the metabolic trap hypothesis might tie into one another.
Maybe that could be a video topic that Ron could take up? @Janet Dafoe (Rose49)
I have many markers for an increased risk of auto-immune diseases and have family members with them (MS, ulcerative colitis, Hashimoto's)...is anyone aware of survey/study data showing that PwME tend to come from families with histories of auto-immunity?
Anecdotally, we hear this a lot. Maybe we could start a poll though statistically our polls are not very accurate--still it would be interesting.
 

jpcv

Senior Member
Messages
386
Location
SE coast, Brazil
I think Davis`work,along with the data from Naviaux and others who are studying metabolome, are the most important in the research of ME/CFS
 

Janet Dafoe

Board Member
Messages
867
I am so appreciative of all of this research - it is truely amazing; but I didn't hear anything different to what was said at the symposium last year? Please correct me if I am wrong...
We now have one of Mark's post-docs working on this, I think full time. And the funding to do it. I know the post-doc has presented at one of their weekly meetings, and everyone thought he was great. I don't know what he has done past what Mark talked about, but I know that he has been doing things. Sorry for not much info, but it is progress to have a whole new person and the funding for the project to move forward. Funding is always the rate limiting step so far.
 

Hopeful1976

Senior Member
Messages
345
We now have one of Mark's post-docs working on this, I think full time. And the funding to do it. I know the post-doc has presented at one of their weekly meetings, and everyone thought he was great. I don't know what he has done past what Mark talked about, but I know that he has been doing things. Sorry for not much info, but it is progress to have a whole new person and the funding for the project to move forward. Funding is always the rate limiting step so far.
I wonder why Mark isn't working on it himself?
Thanks for feeding back - I felt a little disheartened seeing the video in that nothing seemed to have been done in nearly a year...

Could the clonal t cells be something to do with gut bacteria permiating the gut wall (or a specific bacteria/virus) and the immune system battling it constantly... I ask because I have symptoms worsen when my gut symptoms are bad.
 
Messages
88
I wonder why Mark isn't working on it himself?
Thanks for feeding back - I felt a little disheartened seeing the video in that nothing seemed to have been done in nearly a year...

Could the clonal t cells be something to do with gut bacteria permiating the gut wall (or a specific bacteria/virus) and the immune system battling it constantly... I ask because I have symptoms worsen when my gut symptoms are bad.

I was a grad student before I got ME/CFS. From my experience professors typically are more like managers who oversee the research of their lab. Most research is done by grad students and post docs. The profs usually oversee their work, give them ideas, write proposals for funding, teach classes, do peer review of journals, look over admissions, etc.
 

jpcv

Senior Member
Messages
386
Location
SE coast, Brazil
I wonder why Mark isn't working on it himself?
Thanks for feeding back - I felt a little disheartened seeing the video in that nothing seemed to have been done in nearly a year...

Could the clonal t cells be something to do with gut bacteria permiating the gut wall (or a specific bacteria/virus) and the immune system battling it constantly... I ask because I have symptoms worsen when my gut symptoms are bad.
Or the other way around?
For me, my gut worsens when I have a crash
 

raghav

Senior Member
Messages
809
Location
India
Is the t-cell sequence in the clonal expansion the same in all the patients or is it a different seqeunce in different patients ?