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Longitudinal Cytokine and Multi-Modal Health Data of an Extremely Severe ME/CFS Patient with HSD Reveals Insights into Immunopathology, and Disease

Violeta

Senior Member
Messages
2,938
Currently abstract only:
https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2024.1369295/abstract

Jahabani, Ron Davis, Whitney Dafoe, Janet Dafoe, etc

Our longitudinal cytokine profiling underscores the significance of Th2-type cytokines and synergistic activities between mast cells and eosinophils, leading to skewing of Th1 toward Th2 immune responses in ME/CFS pathogenesis, especially in cognitive impairment and sensorial intolerance.
 

Violeta

Senior Member
Messages
2,938
This is from selfdecode dot com.

Isn't it interesting that their study of cytokines seems to have supported this?
1712066498360.png
 

Violeta

Senior Member
Messages
2,938
From the abstract:

"Our longitudinal cytokine profiling underscores the significance of Th2-type cytokines and synergistic activities between mast cells and eosinophils,"

From this study:
https://www.nature.com/articles/mi2012112

Some effects are hypothesized to stem from the main Th2 cytokine, IL-4, and IgE antibodies. These are claimed to stimulate mast cells to release histamine, serotonin, and leukotriene to cause airway constriction and intestinal peristalsis.

From this study:

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7759531/

Mast cells and basophils, activated by IgE, are key sources of IL-4 that tilts the immune balance away from tolerance and towards type 2 immunity by promoting the induction of Th2 cells along with the innate effectors of type 2 immunity, ILC2s, while suppressing the development of regulatory T cells and driving their subversion to a pathogenic pro-Th2 phenotype. This adjuvant effect of mast cells and basophils is suppressed when inhibitory signals are delivered by IgG antibodies signaling via FcγRIIb. This review summarizes current understanding of the immunoregulatory effects of mast cells and basophils and how these functions are modulated by IgE and IgG antibodies. Understanding these pathways could provide important insights into innovative strategies for preventing and/or reversing food allergy in patients.
 

Violeta

Senior Member
Messages
2,938

The effect of kefir consumption on human immune system: a cytokine study

https://pubmed.ncbi.nlm.nih.gov/236...pressing neutrophil chemotaxis and activation.

These results indicated that kefir use increased polarization of the immune response towards TH1 type and decreased TH2 type response and accordingly allergic response. The decrease in IL-8 level due to kefir use, might control the inflammatory response by suppressing neutrophil chemotaxis and activation. On the other hand it was also concluded that increased IL-5 might stimulate secretory IgA at gastrointestinal mucosa leading to a more efficient immune response in the intestinal lumen.
 

Violeta

Senior Member
Messages
2,938

Modulation of Th1/Th2 Cytokine Balance by Quercetin In Vitro​


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7459988/

Allergic rhinitis (AR) is well known to be an IgE-mediated chronic inflammatory disease in the nasal wall, which is primarily mediated by Th2-type cytokines such as IL-4, IL-5, and IL-13. Although quercetin is also accepted to attenuate the development of allergic diseases such as AR, the influence of quercetin on Th2-type cytokine production is not well understood. The present study was designed to examine whether quercetin could attenuate the development of AR via the modulation of Th2-type cytokine production using an in vitro cell culture technique.

The present results strongly suggest that quercetin modulates IL-4-mediated immune responses, especially Th1/Th2 cytokine balance, and results in attenuation of the development of allergic immune responses.
 

Oliver3

Senior Member
Messages
863
Quercetin when I first took it made me feel like a million bucks....stopped my anxiety etc.
Sadly that's not the same reaction, tho it does still help.
Black seed oil was even better for about six months. Total elimination of pots for that time. Endurance uetc.
 

Violeta

Senior Member
Messages
2,938

Oliver3

Senior Member
Messages
863
Hi there...rishi made me really depressed.
Lions mane. Short term benefits.
Before doesn't seem to do anything.
Astralagus some mild beneficial effects.
Also use broccoli sprout extract.
Gingko biloba helps too.

Thanks for the suggestions tho.
It seems we're all trying similar stuff and it seems to help a bit.

I also take allevia , especially during pem

And nattokinase. That helped loads at first.

It's a Shame all these intervention s work for a bit and then lost most of their power. That push towards autoimmunity seems really strong tho doesn't it?

I'm glad room is seeing a link here but a bit perturbed that most of us have got here years ago.

I used to be designated driver when I was a teacher. I'd drink a few pints of fresh orange juice in the night. I felt like I'd been rejuvenated.
I asked my doctor. They said it was sugar...but no other sugars got to it. That's when I started looking into MCAS, like 15 years ago.
These supps have probably kept me out of anaphylaxis but I'm getting increasingly worried as they supps are getting less effective.

Black seed oil is the best of the lot but I darent use it because of the high ratio of omega 6 and 9s. After 6 months, it changed my body a bit so I gave it up.
I've tried black seeds and they're a bit like a quercetin buzz but not as strong.

The most recent thing is nicotine. It really helps with mast cells and dopamine but it's too deleterious long term to keep using.
I really can't see how we can get much further along with these kindve supps. I mean they help and maybe a less ill person could reverse the illness but so frustrating . We need something a bit more radical
 

Violeta

Senior Member
Messages
2,938
@Oliver3, I so agree, this isn't a new topic. I guess the thing about it that's interesting is they have the specific cytokines to prove the point. I guess they are going to make some recommendations of remedies. Hopefully it won't just be another study that says X is wrong, we, ourselves must find the solution.

It is a shame, and strange, too, that so many of us find that most interventions help for a while and then lose their power.

Do you still drink the orange juice. I have done that for a season, it felt like such a relief while drinking it. I wasn't sure if it was making me feel much worse in the morning, so I've quit, at least for a while.

Do you have difficulty finding food that doesn't bother you? The list of foods I can eat is so short, and I frequently end up having to change what I am eating. I think that's the most difficult thing for me right now.

Have you tried CBD oil? It has helped me with a couple of symptoms, and I have to get back to taking it regularly. Starting tonight.

Have you tried kefir? I am putting a lot of hope into that making some sort of positive change in my condition.
 

Oliver3

Senior Member
Messages
863
I agree with you, it's more proof of context that the omf are doing.
CBD really doesn't agree with my vascular system. I've tried it loads and edibles.
Increases my anxiety too. But everyone is different.
I don't think orange juice is a good way forward cos if the sugar and the effect on my bones. But that's why flavonoids like quercetin are so good.

God yeah, my stomach doesn't like many foods...I have constant reflux too. Pretty miserable.

I've tried kefir but not long term I guess I could give it another go. It just seemed to do nothing when I took it but I didn't give it long enough.

When I'm feeling stronger, I actually fast, which is probably not a good idea but it's a relief from all the reactions
 

Oliver3

Senior Member
Messages
863
That's great it's been done...also..mad how most of us had put a lot of this together ourselves, whilst being gaslit the entire time by the so called professionals
 

Violeta

Senior Member
Messages
2,938
That's great it's been done...also..mad how most of us had put a lot of this together ourselves, whilst being gaslit the entire time by the so called professionals
I agree. And I don't know if those who wrote it even have any way of helping us out of this h*ll.
 

leokitten

Senior Member
Messages
1,578
Location
U.S.
@Janet Dafoe congrats on the paper. Have you and Ron thought about interleukin-2 inducible T-cell kinase (ITK) inhibition as a target for ME/CFS? If ME is a T-cell mediated inflammatory/immune disease with a Th2 skew this could be a promising target. Soquelitinib (formerly known as CPI-818) for example is a selective ITK inhibitor that modulates affected cells back towards a Th1 phenotype and has demonstrated efficacy in Th2 mediated diseases in preclinical models. I believe they’ve also done some early stage human trials with it in cancer and atopic dermatitis.
 
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gm286

Senior Member
Messages
149
Location
Atlanta, GA
My IL2R was considered "high" / scored for "high concentration" on an immune urinary analysis many years ago. Not sure if relevant but inserting it in here anyway.

"CD4/CD25+" lymphocytes were measured at 1mm3 for a normal reference range of 52-255.
Not sure what it means to have high IL2R but low CD25, thought they were supposed to correlate positively.

Screenshot 2024-04-11 at 2.25.02 PM.png


Screenshot 2024-04-11 at 2.21.18 PM.png
 

leokitten

Senior Member
Messages
1,578
Location
U.S.
ITK inhibitors in inflammation and immune-mediated disorders, Sahu et al, 2009
Interleukin-2-inducible T cell kinase (ITK) is a non-receptor tyrosine kinase expressed in T cells, NKT cells and mast cells which plays a crucial role in regulating the T cell receptor (TCR), CD28, CD2, chemokine receptor CXCR4, and FcepsilonR-mediated signaling pathways. In T cells, ITK is an important mediator for actin reorganization, activation of PLCgamma, mobilization of calcium, and activation of the NFAT transcription factor. ITK plays an important role in the secretion of IL-2, but more critically, also has a pivotal role in the secretion of Th2 cytokines, IL-4, IL-5 and IL-13. As such, ITK has been shown to regulate the development of effective Th2 response during allergic asthma as well as infections of parasitic worms. This ability of ITK to regulate Th2 responses, along with its pattern of expression, has led to the proposal that it would represent an excellent target for Th2-mediated inflammation. We discuss here the possibilities and pitfalls of targeting ITK for inflammatory disorders.