Playing armchair scientist for a minute in an atte
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Posted On: 06/25/2021 2:31:24 PM
Playing armchair scientist for a minute in an attempt to stitch together all that was said or alluded to. Would appreciate some feedback...
There are two arms to the immune system, the innate and the adaptive. The innate is the less intelligent (non-specific) arm. It's the first line of defense against something like COVID since the threat is novel. This is where macrophages come into play. They phagocytize the virus.
The adaptive side of the immune system is the more precise arm of the immune system. This is where T-cells and B-cells come into play. T-cells receive information from the innate side via antigen presenting cells (APCs). APCs encounter the threat (i.e. COVID) and take a piece of it (an epitope), absorb it and present that to a T-Cell. The T-Cell is then activated, natural killer cells (NK) upregulate. T-Cells in turn trigger B-Cells which in turn produce antibodies. The antibodies create the specific immune response to the threat (i.e. COVID).
The innate response creates an inflammatory state as the body attempts to fight off the invader. However, for some individuals this inflammatory response persists. Why? Dr. Patterson mentioned that there is something different occurring in LHers where these monocytes carrying the spike protein live long past their normal lifespan causing this inflammatory state to persist but he didn't dive into what that was.
Is this due to human leukocyte antigen (HLA)? HLA is the genetic encoding on chromosome 6 that is responsible for encoding cell-surface proteins (https://en.wikipedia.org/wiki/Human_leukocyte_antigen). Differences in this encoding have been thought to play a role in post-lyme, chronic inflammation response syndrome (CIRS), etc. The basic science as I understand it is that if one has the errant encoding they may have compromised antigen presentation which then leads to being stuck in this inflammatory innate response without the specific adaptive response taking over.
What is interesting with regards to CIRS is that the percentage of the population estimated to suffer from CIRS due to genetic factors of HLA are 24% which reminded me of the 20-30% estimate for LHers (https://fibromyalgiafortmyers.com/genetics-and-cirs/)
What does this have to do with Leronlimab? If what I am stating is in fact correct, I believe that our market for inflammatory conditions encompasses all disesease that are linked to defects in HLA. It was eye opening to me to learn that this is not just about LHers or Chronic Fatigue Syndrome but potentially about all the conditions caused by the defects in APCs that lead to individuals being stuck in the innate phase of the immune response when confronted with novel pathogens. This can occur to contact with biotoxins (i.e. mold), bacteria and/or viruses. Perhaps it is involved in the post vaccine reactions some are having as well.
Anyhow, fascinating stuff! Even if I am way off, I am learning a ton on this journey :- ) Thanks to all who have shared their discoveries as well!
There are two arms to the immune system, the innate and the adaptive. The innate is the less intelligent (non-specific) arm. It's the first line of defense against something like COVID since the threat is novel. This is where macrophages come into play. They phagocytize the virus.
The adaptive side of the immune system is the more precise arm of the immune system. This is where T-cells and B-cells come into play. T-cells receive information from the innate side via antigen presenting cells (APCs). APCs encounter the threat (i.e. COVID) and take a piece of it (an epitope), absorb it and present that to a T-Cell. The T-Cell is then activated, natural killer cells (NK) upregulate. T-Cells in turn trigger B-Cells which in turn produce antibodies. The antibodies create the specific immune response to the threat (i.e. COVID).
The innate response creates an inflammatory state as the body attempts to fight off the invader. However, for some individuals this inflammatory response persists. Why? Dr. Patterson mentioned that there is something different occurring in LHers where these monocytes carrying the spike protein live long past their normal lifespan causing this inflammatory state to persist but he didn't dive into what that was.
Is this due to human leukocyte antigen (HLA)? HLA is the genetic encoding on chromosome 6 that is responsible for encoding cell-surface proteins (https://en.wikipedia.org/wiki/Human_leukocyte_antigen). Differences in this encoding have been thought to play a role in post-lyme, chronic inflammation response syndrome (CIRS), etc. The basic science as I understand it is that if one has the errant encoding they may have compromised antigen presentation which then leads to being stuck in this inflammatory innate response without the specific adaptive response taking over.
What is interesting with regards to CIRS is that the percentage of the population estimated to suffer from CIRS due to genetic factors of HLA are 24% which reminded me of the 20-30% estimate for LHers (https://fibromyalgiafortmyers.com/genetics-and-cirs/)
What does this have to do with Leronlimab? If what I am stating is in fact correct, I believe that our market for inflammatory conditions encompasses all disesease that are linked to defects in HLA. It was eye opening to me to learn that this is not just about LHers or Chronic Fatigue Syndrome but potentially about all the conditions caused by the defects in APCs that lead to individuals being stuck in the innate phase of the immune response when confronted with novel pathogens. This can occur to contact with biotoxins (i.e. mold), bacteria and/or viruses. Perhaps it is involved in the post vaccine reactions some are having as well.
Anyhow, fascinating stuff! Even if I am way off, I am learning a ton on this journey :- ) Thanks to all who have shared their discoveries as well!
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