Discussion in 'Immunological' started by lnester7, Jan 6, 2013.
CD4 T cells perhaps.
I have low numbers. As far as I know, activation was not tested. Thanks for the links!
I was told it doesn't treat CD8 dysfunction.
The hope is that CD8 numbers will improve as we clear all the infections (and keep them under control). As I understand it, low CD8 numbers can occur with immune exhaustion, so that's what we're hoping is going on.
I have long wondered if some of the success of general anti-pathogenic treatments including antibiotics and antivirals might exert some of their effect in some patients by lowering pathogen load, giving the immune system more time to rest. It might not be really treating a specific pathogen, just lowering total burden.
Cheney recommends the following to help shift the immune system from one mode to another. They are called "right to left shifters". Three of them are published, or near publication.
) Pine Cone Extract. Cheney said, "They make a tea from this in Southern Japan and they have significantly reduced cancer rates. It's thought to work at the gene level in lymphocytes, where it turns on IL-12. It also shuts down IL-10 at the gene level, and that causes a shift towards Th1. Pine Cone extract is expensive, but at just 10 drops a day (in the morning), of all the possibilities, it's probably the cheapest per day." It is called PineExtra, and 1 oz is about $60, but it lasts a long time.
Dare i ask, anyone tried Pine cone extract?
There are a lot of Th2 ➤ Th1 shifting supplements in addition to pine cone extract, including those listed here and here.
I have experimented with simultaneously taking around a dozen of the most potent Th2 ➤ Th1 shifters listed in those above weblinks, in order to create a massive shift to Th1 in my body.
However, I unfortunately found that in my case, taking certain Th2 ➤ Th1 shifters causes considerable depression symptoms as a side effect, so I was unable to continue. The Th2 ➤ Th1 shifting supplements that seem to provoke the most depression in me were: Epicor (Saccharomyces cerevisiae), Astragalus, inosine, beta sitosterol, and transfer factor.
But for other people here that want to experiment, I think taking a whole stack of these Th2 ➤ Th1 shifters together might be a very good way to treat ME/CFS, which is considered a Th2-dominant disease.
Dr Nancy Klimas often prescribes the Th2 ➤ Th1 shifter Imunovir to her ME/CFS patients, and Dr John Chia often prescribes the Th2 ➤ Th1 shifter oxymatrine; but why take just one of these shifters? Why not take a dozen?
Though if you want to shift from Th2 to Th1 in this way, it is a good idea to also treat any EBV, CMV or HHV-6 active infections you may have, as according to Dr Cheney, all these three viruses make a fake version of IL-10, a cytokine which shifts the immune response towards the undesirable Th2 (ref: here). Indeed, it could well be that active EBV, CMV or HHV-6 infections are primarily responsible for the undesirable Th2 dominance in many cases of ME/CFS. I would think that unless you address this ability of EBV, CMV or HHV-6 to shift towards Th2, you will be swimming against the current if you just take Th2 ➤ Th1 shifting supplements.
The bacterial toxin LPS (lipopolysaccharide) causes an undesirable shift to Th2 as well. LPS comes from Gram negative bacteria in the gut, and if you have a leaky gut, some researchers think this LPS can escape from the gut into the bloodstream, where it then acts systemically to shift to the undesirable Th2 side. So as part of any Th2 ➤ Th1 shifting protocol, you would want to make sure you have not got any gut dysbiosis, SIBO or leaky gut that may be pumping out LPS into your bloodstream.
High cortisol will shift to the undesirable Th2 too, so you would want to take supplements like phosphatidylserine to lower your cortisol if it is high.
In summary: in order to shift from Th2 to Th1, it may be a good idea to take lots of Th2 ➤ Th1 shifting supplements simultaneously; but you also need to address factors such as active EBV, CMV or HHV-6 infections, excess LPS production from gut dysbiosis, SIBO or leaky gut, and high cortisol, as these factors all shift to the undesirable Th2 side.
In this video, Dr Chia talks about his use of the immunomodulator oxymatrine on his ME/CFS patients (see timecode 31:25).
If low cortisol is a problem for many ME sufferers mightn't that again be linked to an overactive immune system, since cortisol acts to suppress immune responses?
Thanks I read it. I have a few basic questions:
Is there any independent data on what percentage of tested patients manifest this T-shift he theorises?
Is there any data on how effective his treatment protocol is?
Is there any data to suggest ME sufferers are predisposed to get cancer?
How does this theorised T-shift and consequent susceptibility to infection square with those like myself who report, au contraire, a very high resistance to viral and bacterial infection?
Lastly and most importantly - if a degree of immune collapse was really part of the causative agency, I can't imagine the compensation process he theorises would work indefinitely, so wouldn't we expect to see extreme cases of almost total immune-collapse leading to AIDS-like syndromes? But so far as I know we don't see this do we?
My illness always improves on antibiotics, even though most of the time I get them for some other complaint. So this might make sense, at least for me.
On cancer risk, it has long been suspected and even in the 1980s Komaroff tried to get funding to do proper epidemiology on this. No funding was ever forthcoming. Recently a paper confirming the risk was published:
Some of us do have severe immune collapse. Some of us have HIV-like syndromes, but without HIV, and not as progressive. There are even anecdotal reports of issues like Karposi's sarcoma, which is typically only found in AIDS patients. Certain kinds of infections we are particularly susceptible to due to our poor NK function - this is documented to lead to cancer, fungal infections and herpes virus infections, iirc, in non-CFS patients. Why should we be different? However this whole area is massively underfunded - we could use better data.
On LPS I hope to write a blog on this later this year. I don't think dysbiosis has much to do with it, except that LPS is NOT one single chemical, its a family, and different bacterial species produce different forms of it. Somehow LPS gets into our bloodstream. This should never happen, and indicates multiple failures in the immune system.
From personal experience, I have always perceived this as an AIDS-like syndrome. But it always baffled me why doctors look right past me when I am at my worst. And I end up having to treat myself with antibiotics to get back to baseline.
Maybe you have something different? Or just less severe.
I am 26 and this feels like this can definitely take my life if I let it - but I try not to go down that path of thought anymore.
Thats a good summary and good links.
The reason why we are not suppose to take all of them at the same time, is basically the capacity of the body to fight whatever you are getting out! So if you are chelating metals by using methylation or Mega C, but you go to a faster pace that you body can process, then you will crash instead of getting better. That was the explanation my Dr gave me. I am desperate because she starts me in one pill at the time (Except the vitamins) and she starts me on very low doses, even though I am not one of those sensitive to pills type.
She tells me I didn't get like this in one day (I have been sick for 5 years) so don't expect to clear it all in one.
Today I have CFS and I do suffer, Is hard to explain but you know when you suffer of thyroid and they fix that or sleep. You feel that a part of the puzzle has been fixed? That is what I felt on all the immune modulator. I am not cured, but I don't feel with the flue 24/7. I get my labs soon, will let you know where I am on the shift.
Let's not forget that it's not just a Th2/Th1 thing. Someone fairly recently (~5 years) discovered a Th-17 pathway (?) which may be a big player in ME/CFS. "Low Th-17 levels may leave the host susceptible to to opportunistic infections" according to my immune report.
Yes that is true; we should really be talking about the Th1— Th2 — Th17 immune balance, not just the Th1 — Th2 balance.
I have been looking into the Th17 immune response and its role in ME/CFS. Like Th1, the Th17 immune response has also been found to be low in ME/CFS, at least in this study; but from what I can tell, it seems that Th17 might be undesirable in ME/CFS anyway, for the following reasons:
This study say that Th17 cells are implicated in allergic inflammation, intestinal diseases, central nervous system inflammation. The study found that ME/CFS patients tend to possess genetic alleles that cause a higher, more pro-inflammatory TH17 immune response, and the study concludes that Th17 may play a role in the pathogenesis of CFS.
This study says that Th17 cells contribute to coxsackievirus B3 replication (in CVB3 myocarditis). Since coxsackievirus B is strongly associated with ME/CFS, anything that boosts its replication can't be good.
N-acetylglucosamine (NAG) reduces the Th17 response, incidentally. I found taking NAG greatly reduces my anxiety symptoms.
Th-17 ? Good grief. More stuff to google
It was something many ME specialists had said in the past about non-Hodgkin lymphoma and ME/CFS and fortunately a study was finally done which also showed what they'd been saying about noticing an increased risk.
Note..they did that study on elderly CFS people. I wonder what the results would of been had they instead compared those who had ME (international definition) and had had ME long term.. eg at least 10 years with a matched age/sex control group who werent elderly. Some of our ME experts have seen also a type of very rare brain cancers in those who have ME (I think I remember hearing that one specialist had 3 ME patients with this very very rare cancer).
ME/CFS at one point was being called.. non HIV AIDS due to the immune abnormalities which can appear in a subgroup of ME/CFS people
There are something like 7 different helper T cells, with several other cell types that mimic them or have redundant function. The immune system is still not fully understood, and the science will probably reveal a few more surprises in time.
Those Th17 mimics may include gamma delta T cells, which is a topic I am currently investigating:
V4+ T cells act as TH-17 cells in a mouse model of collagen-induced arthritis
Christina Roark1, Jena D. French1, Molly A. Taylor1, Alison M. Bendele2, Willi K. Born1 and Rebecca L. O’Brien1
Confused.....has Th-17 been found to be decreased or increased in those with CFS/ME in more studies? I looked into Th-17 awhile ago, and my brain isn't remembering what I learned.
I thought Th-17 levels from my lack of effective memory, were raised, in which correlates with the epithelial and mucosal problems common in CFS/ME? And with my learning endeavors into interferon and its relation, deletion of interferon genes, would then affect the level of Th1 T cells, and initiate a Th2 dominance and a lack of control of the Th17???
This immune stuff boggles my mind.
Looking at the first link alex3619 gave us, I see something that sure sounds like my situation:
along with the following diagram.
Th17 Cell Lineage Diagram
I have low (10-25%) IL-17 and very low (<10%) IL-23 which certainly suggests ROR gamma T (whatever that is) deficiency. Now if only I had a clue what that means for me in terms of health, treatment, or anything useful. **sigh**
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