Post by brantheman on May 17, 2024 6:35:25 GMT -8
I seem to be the biggest fan of digging in mud, formerly known as diagnostic markers for immune dysruption.
Jokes aside the field of immune dysruption in ME/CFS, Long Covid, Mold, CIRS, Chronic Lyme, Bartonellosis etc has interested me the most because in my understanding its the root of the issue.
Why are our bodies susceptible to pathogens that a human being without immune dysruption could clear? This is a question that has never settled in me. The search for an answer is burning like a flame in me. If we were able to understand the complexity of our immune system by the fullest we could cure millions. Millions that are currently bedbound, missing as a father, mother, son or daughter. Millions of friends, millions people currently missing out on life because of severe health issues our government have absolutely 0 interest in curing. It seems more lucrative to keep people ill.
I am not a specialist in any way and I still don't understand lots of things but I can try to give people a basic understanding of this topic.
Today I want to start about the Th1-Th2-Th17 Topic.
First of all, what does Th stand for? It stand for T-helper Cell. These T helper cells produce different cytokines (signals) that tell our other immune cells what they have to do.
Thats why they are pretty important and can tell us a lot about the immune system functionality.
Not too long ago we had a strict system that tried to devide the T-Helper Cells or short Th in 2 Categories:
Th1 and Th2. Th1 Being responsible for a cellular immunity and Th2 being responsible for an antigen presenting immunity aswell as the responsibility to fight of parasites like leishmania etc.
What we know today is that there are a lot more Thelper classes going on. There has been so far identified: Th1, Th2, Th17, Th9, Th22 and Treg. (more to come haha)
The most information seems to be available about Th1, Th2, Th17 and Treg so we will focus on that today.
Th1 Cells are responsible for cellular immunity as for example intracellular bacteria (e.g. lyme) and viruses like cytomegalie-virus. The Th1 Cell and its cytokine target and activate Macrophages and Dedritic Cells. This may be the reason some ME/CFS individuals report improvements from GcMAF because its a macrophage activating peptide that kinda works around the (commonly) dyfunctional th1 immnity in ME/CFS individuals.
Th2 Cells are responsible for humoral immunity as for example antigen production, allergens and parasites. Their target are B-Cells, Eosinophils and Basophils. Th2 is commonly elevated in some ME/CFS and chronic lyme individuals but this is not a consistent finding. Th2 can be increased through a few mechanisms that we may discuss in an other thread. Th2 loss can result in recurrent parasitic infections, loss of humoral immunity etc.
Th17 Cells are responsible for extracellular bacteria as for example staph infections and fungal infections like c. albicans, but their overexpression are heavily linked to autoimmunity so Th17 has a sweet spot. We want it just right, not too low and not too high. Th17 Cells and their Cytokines target Neutrophils and Epithelial cells.
phoenixrising.me/myalgic-encephalomyelitis-chronic-fatigue-syndrome/lipkin-finds-biomarkers-not-bugs/ In a 2013 study, Lipkin found that IL-17 depletion seems to be a common finding in ME/CFS patients sick for 3< years. Patients <3 years of illness tended to have elevated levels. So there seems to be some kind of immune exhaustion taking place.
Treg Cells are as the name might suggest responsible for a sort of regulatory function. It tries to dampen down overreactive parts of other system. If we would imagine the immune system as a car Treg would be considered the brake. Its job is to tell the other immune system parts that their job is done and they can chill out. Their main target are APC and effector cells.
This still needs some editing but Imma post this with the hint that its: currently under construction.
Jokes aside the field of immune dysruption in ME/CFS, Long Covid, Mold, CIRS, Chronic Lyme, Bartonellosis etc has interested me the most because in my understanding its the root of the issue.
Why are our bodies susceptible to pathogens that a human being without immune dysruption could clear? This is a question that has never settled in me. The search for an answer is burning like a flame in me. If we were able to understand the complexity of our immune system by the fullest we could cure millions. Millions that are currently bedbound, missing as a father, mother, son or daughter. Millions of friends, millions people currently missing out on life because of severe health issues our government have absolutely 0 interest in curing. It seems more lucrative to keep people ill.
I am not a specialist in any way and I still don't understand lots of things but I can try to give people a basic understanding of this topic.
Today I want to start about the Th1-Th2-Th17 Topic.
First of all, what does Th stand for? It stand for T-helper Cell. These T helper cells produce different cytokines (signals) that tell our other immune cells what they have to do.
Thats why they are pretty important and can tell us a lot about the immune system functionality.
Not too long ago we had a strict system that tried to devide the T-Helper Cells or short Th in 2 Categories:
Th1 and Th2. Th1 Being responsible for a cellular immunity and Th2 being responsible for an antigen presenting immunity aswell as the responsibility to fight of parasites like leishmania etc.
What we know today is that there are a lot more Thelper classes going on. There has been so far identified: Th1, Th2, Th17, Th9, Th22 and Treg. (more to come haha)
The most information seems to be available about Th1, Th2, Th17 and Treg so we will focus on that today.
Th1 Cells are responsible for cellular immunity as for example intracellular bacteria (e.g. lyme) and viruses like cytomegalie-virus. The Th1 Cell and its cytokine target and activate Macrophages and Dedritic Cells. This may be the reason some ME/CFS individuals report improvements from GcMAF because its a macrophage activating peptide that kinda works around the (commonly) dyfunctional th1 immnity in ME/CFS individuals.
Th2 Cells are responsible for humoral immunity as for example antigen production, allergens and parasites. Their target are B-Cells, Eosinophils and Basophils. Th2 is commonly elevated in some ME/CFS and chronic lyme individuals but this is not a consistent finding. Th2 can be increased through a few mechanisms that we may discuss in an other thread. Th2 loss can result in recurrent parasitic infections, loss of humoral immunity etc.
Th17 Cells are responsible for extracellular bacteria as for example staph infections and fungal infections like c. albicans, but their overexpression are heavily linked to autoimmunity so Th17 has a sweet spot. We want it just right, not too low and not too high. Th17 Cells and their Cytokines target Neutrophils and Epithelial cells.
phoenixrising.me/myalgic-encephalomyelitis-chronic-fatigue-syndrome/lipkin-finds-biomarkers-not-bugs/ In a 2013 study, Lipkin found that IL-17 depletion seems to be a common finding in ME/CFS patients sick for 3< years. Patients <3 years of illness tended to have elevated levels. So there seems to be some kind of immune exhaustion taking place.
Treg Cells are as the name might suggest responsible for a sort of regulatory function. It tries to dampen down overreactive parts of other system. If we would imagine the immune system as a car Treg would be considered the brake. Its job is to tell the other immune system parts that their job is done and they can chill out. Their main target are APC and effector cells.
This still needs some editing but Imma post this with the hint that its: currently under construction.