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Also, if you do not think the term should be used in this context, would you therefore say that it is not possible/useful to broadly characterise the differences between the immune systems of different individuals, sexes, or species?
Well, I was just defending idea of a proinflammatory/antinflammatory balance (or immunosignature) which you said was immunobabble. I brought it up because I think that some people (especially those on this forum) might actually be thinking of such a balance/signature when they talk about Th1/Th2. I cannot say for sure what Lipkins means by it, since as he doesn´t visit this forum I am not able to ask him.
The chronic active infections linked to ME/CFS are intracellular infections, so the theory goes that you need the Th1 branch to fight these. The idea is that ME/CFS patients might be shifted towards Th2, thus preventing them from mounting a good Th1 response. But as I said, the Th1 and Th2 responses are not that polarized in humans, so the validity of the Th1/Th2 balance in ME/CFS needs to be questioned.
The immune modulator I use shifts the response more towards Th1
Have you noticed any symptom improvement?
I was dying and after I started taking the immunemodulator I very slowly imporved.
Many symptoms disappeared and others decreased. I am not cured but muxh better.
That sounds like a big improvement! Anything that gives a significant improvement is always welcome! You must have been pleasantly surprised?
th1 arm becomes exhausted over time, leaving a higher th2.
This is what happens in T cell exhaustion. As the cells become more and more downregulated, they stop producing th1 cytokines.I have never come across a "Th1 exhaustion" hypothesis. Did you read about this somewhere?
@msf, the Th1/Th2 balance idea does not refer to a pro-inflammatory / anti-inflammatory balance, but rather to the relative activations of two different branches of the immune response: the Th1 branch, which targets intracellular infections (such as viruses and intracellular bacteria like Chlamydia pneumoniae), and the Th2 branch, which targets extracellular infections like bacteria.
I understand that in mice, the Th1 and Th2 responses are quite mutually exclusive and polarized, so that when Th2 is engaged, it prevents the engagement of Th1, and vice versa. In other words, you cannot have both Th1 and Th2 at the same time.
This is how the idea of the Th1/Th2 balance came into being. The idea is that if the Th1 side of the seesaw is raised, then the Th2 side will be lowered. So the idea is that you cannot effectively fight both Th1 and Th2 infections at the same time, at least im mice.
But it turns out that in humans, the Th1 and Th2 responses are not as polarized and mutually exclusive as they are in mice, so the idea of seesaw balance does not apply as much to humans. Humans are more able to raise both sides of the seesaw at the same time.
The way that the Th1/Th2 balance has been applied to ME/CFS is as follows:
The chronic active infections linked to ME/CFS are intracellular infections, so the theory goes that you need the Th1 branch to fight these. The idea is that ME/CFS patients might be shifted towards Th2, thus preventing them from mounting a good Th1 response. But as I said, the Th1 and Th2 responses are not that polarized in humans, so the validity of the Th1/Th2 balance in ME/CFS needs to be questioned.
Certainly though enteroviral persistence is associated with ongoing ME/CFS, and enteroviral clearance or reduction in enteroviral loads is associated with remission or amelioration in ME/CFS symptoms. Dr Chia has found that with his oxymatrine, ribavirin and interferon treatments for ME/CFS, enteroviral loads went down as ME/CFS symptoms abated. And Dr Chia did show that enteroviral clearance from oxymatrine treatment was associated with an increase in the IL-12 / IL-10 ratio (these are Th1 and Th2 cytokines respectively), which implies an increase in the Th1/T2 ratio.
So although the validity of the Th1/Th2 balance in ME/CFS needs to be questioned, the general idea that there is something in ME/CFS patients' bodies or immune system that is preventing viral clearance still remains. If we can figure out what this assumed blocking factor is that prevents viral clearance, we may be able to find a cure for ME/CFS.
This assumed blocking factor is also relevant to chronic enteroviral myocarditis, where an acute enteroviral infection of the heart muscle does not resolve in some patients, but remains as a chronic persistent infection.
Over the years, I have been on the lookout for possible explanations of why an infection fails to resolve, and remains persistent.
This is what happens in T cell exhaustion. As the cells become more and more downregulated, they stop producing th1 cytokines.
Highlights
- Persistent viral infections can result in the exhaustion of anti-viral T cells.
- Excessive and sustained levels of viral antigen drive T cell exhaustion.
- Exhausted T cells are distinct from typical effector and memory subsets.
- Exhausted T cells are functionally ineffective and compromise viral clearance.
- Blocking inhibitory receptors and modifying cytokine levels can alleviate exhaustion.