Thank you so much for these explanations with the complex science broken down to elements that help those of us without biology education to begin to grasp the process; it's awesome help!!
Great series. I appreciate your simplified explanations. And those Janeway’s Immunobiology graphics are the best!
Question (for anybody here). I recall reading fairly early on in the C19 pandemic, but after the vax had been rolled out for a while, that secretory IgA was diminished or suppressed in the vaccinated. Anyone have any further info on this, or know of any research? And could this be one of the reasons the vaxxed are becoming the more prone Sars-CoV-2 sickened? 🤔
"Suppressed" relative to what? https://www.sciencedirect.com/science/article/pii/S235239642100582X is a pretty good look at this. It shows post-injection responses for both naive and the already infected, so you can compare with the "T0" baseline of the already infected (fig 1). There's no detectable salivary IgA. That's missing a comparison to what would be seen shortly after infection, but clearly IgA fades after a while in natural immunity.
However, then you can see it kick back up after dose 2, much higher than the naive+injected. So the real difference is probably tissue resident IgA-secreting B Cells are left behind by natural infection. Currently tissue resident memory B Cells are understood as the "main source of respiratory IgAs" https://www.frontiersin.org/articles/10.3389/fimmu.2022.953088/full Various sources tend to speculate that BRMs probably expand upon antigen encounter just like circulating memory B Cells, so you go from a faded-out IgA response to a very strong one quickly if the virus comes back, probably.
There's little way to measure infection vs. injection-induced BRMs, but presumably injection isn't going to give you any because there's no way for B Cells to know that spike protein in random organs means "go look for this in respiratory tract." Presumably they are abundant post-infection, though maybe were focused (along with TRMs) on lower respiratory tract in pre-Omicron immune responses, hence why Omicron (tropism for upper respiratory tract) escaped natural immunity. Fig 2 of the first link does seem to show a skew to serum IgA vs. salivary in the naive+injected, so this could reflect lack of tissue localization.
I thought it would be amusing to ask wokeBot (chatGPT) about CDC corruption. Here is the question and answer, featuring the phrases "accused of" and "investigated thoroughly". LOLOLOLOL
"Does the CDC ever engage in corrupt practices to benefit the profits of the Pharma corporations? What about the revolving door between CDC and Pharma? Make it a brief answer."
"There have been instances where individual members of the CDC have been accused of engaging in behavior that could be seen as benefiting the profits of the pharmaceutical industry. However, these instances are typically investigated thoroughly, and the CDC has policies and guidelines in place to prevent conflicts of interest and maintain transparency. A revolving door between the CDC and the pharma industry, where individuals move back and forth between the two, has been a concern in the past, but the CDC has taken steps to address this issue and limit the po tential for conflicts of interest."
It's a good job that the genetic engineers responsible for mRNA "vaccines" and other genetically engineered drugs have an absolutely perfect understanding of the complexities of the immune system and thus the effects of their products upon it.
Otherwise humanity might be in a bit of trouble.
Whatever happened to - It's what you don't know you don't know......
Yes that is clear, and you answered a question about my latest CBC. You didn't tell me anything I didn't already know about the CDC, but that's quite alright. Thank you!
Interesting, thanks. I was under the impression that humoral monocytes extravasate and become M1 or M2 macrophages with the M3 still a bit of an enigma in humans. Also never heard of monocyte/macrophage differentiation into DCs, although aware of DC subsets with DC-5 probably closest to a monocyte.
As for DC origins, here's how I understand it. For awhile both macrophages and DCs were thought to originate from monocytes. Then later some argued that macrophages and DCs derived independently from monocytes and originated from stem cells that were distinct from monocytes. BUT there's been some recent work suggesting that monocytes can also differentiate into DCs (or macrophages). More here on that: https://www.sciencedirect.com/science/article/abs/pii/S1084952117303622
Anyway, my guess is that there are some subsets of DCs that originate from stem cells distinct from monocytes, and some that are derived from monocytes ("mo-DCs" or monocyte-derived DCs). But our understanding of it is still evolving...
Hey Joomi, do you think it would be bad then, if, according to Pfizer's own study #185350, which the FDA tried to hide from the public for 75 years, the mRNA filled LNP's of the vaccine would end up in the bone marrow, detectable there 25 minutes after IM injection and rising in concentration until end of test at 48h after injection (starting at 0.489 accumulating to 3.771 μg lipid equiv/g (mL))? I mean do we want our hematopoietic stem cells to be swimming in a bath of LNPs all waiting to transfect them, producing spike protein only to be targeted then by our own immune system? Does anyone think that that would be a good thing?
Oh, and one question: Has anyone seen any document describing which cell lines the LNP are NOT transfecting? Cause I have searched and so far it seems those LNPs are very UN-targeted.... so fi it its a neuron in your brain, a stem cell in your bone marrow, a cell in your spinal cord, or your heart muscle, the LNPs WILL transfect them, with the consequence being your immune system will kill those cells. So in short:
I mean it's not impossible... I don't think it's something that's very likely given that HSCs make up such a tiny percentage of the cells in the bone marrow... but it's possible...
"However, of approximately 100 cells analysed, only three presented spikes, suggesting low levels of expression."
This could mean there are some cell types that do not express spike (perhaps due to post-translation processing differences that result in spike being scuttled) or that the vial they were testing was full of blanks or truncated RNAs. Anyone's guess.
If I understand it correctly, so far there have not been done any testing on what kind of cells will be able to be transfected (and again, I am pretty sure the LNPs do not differentiate between cell types) and then actually express the spike (this may be different though), though the study you quoted seems to suggest that this expression could be going on for as long as 60 days. And extracellular vesicles with spike on the outside were detected up to 4 months after injection! Here it would be very interesting to see, if those vesicles could lead to syncytia in tissue presenting ACE2... like the endothelial cell lining in every blood vessel in your body (vesicle could fuse with cell-> cell now presenting spike would fuse with neighbors presenting ACE2-> syncytia -> whatever problems would arise from syncytia of cells not normally seen to produce syncytia).
Thank you so much for these explanations with the complex science broken down to elements that help those of us without biology education to begin to grasp the process; it's awesome help!!
Great series. I appreciate your simplified explanations. And those Janeway’s Immunobiology graphics are the best!
Question (for anybody here). I recall reading fairly early on in the C19 pandemic, but after the vax had been rolled out for a while, that secretory IgA was diminished or suppressed in the vaccinated. Anyone have any further info on this, or know of any research? And could this be one of the reasons the vaxxed are becoming the more prone Sars-CoV-2 sickened? 🤔
"Suppressed" relative to what? https://www.sciencedirect.com/science/article/pii/S235239642100582X is a pretty good look at this. It shows post-injection responses for both naive and the already infected, so you can compare with the "T0" baseline of the already infected (fig 1). There's no detectable salivary IgA. That's missing a comparison to what would be seen shortly after infection, but clearly IgA fades after a while in natural immunity.
However, then you can see it kick back up after dose 2, much higher than the naive+injected. So the real difference is probably tissue resident IgA-secreting B Cells are left behind by natural infection. Currently tissue resident memory B Cells are understood as the "main source of respiratory IgAs" https://www.frontiersin.org/articles/10.3389/fimmu.2022.953088/full Various sources tend to speculate that BRMs probably expand upon antigen encounter just like circulating memory B Cells, so you go from a faded-out IgA response to a very strong one quickly if the virus comes back, probably.
There's little way to measure infection vs. injection-induced BRMs, but presumably injection isn't going to give you any because there's no way for B Cells to know that spike protein in random organs means "go look for this in respiratory tract." Presumably they are abundant post-infection, though maybe were focused (along with TRMs) on lower respiratory tract in pre-Omicron immune responses, hence why Omicron (tropism for upper respiratory tract) escaped natural immunity. Fig 2 of the first link does seem to show a skew to serum IgA vs. salivary in the naive+injected, so this could reflect lack of tissue localization.
Thanks! That is very interesting information on the BRM’s.
I thought it would be amusing to ask wokeBot (chatGPT) about CDC corruption. Here is the question and answer, featuring the phrases "accused of" and "investigated thoroughly". LOLOLOLOL
"Does the CDC ever engage in corrupt practices to benefit the profits of the Pharma corporations? What about the revolving door between CDC and Pharma? Make it a brief answer."
"There have been instances where individual members of the CDC have been accused of engaging in behavior that could be seen as benefiting the profits of the pharmaceutical industry. However, these instances are typically investigated thoroughly, and the CDC has policies and guidelines in place to prevent conflicts of interest and maintain transparency. A revolving door between the CDC and the pharma industry, where individuals move back and forth between the two, has been a concern in the past, but the CDC has taken steps to address this issue and limit the po tential for conflicts of interest."
Bought bot.
Joomi, your ability to explain this complex subject clearly is remarkable and way better than every textbook I have come across.
Thanks for this series. The immune system is so complex it's nice to have it broken down. I put a cheat sheet on my phone to refer to.
It's a good job that the genetic engineers responsible for mRNA "vaccines" and other genetically engineered drugs have an absolutely perfect understanding of the complexities of the immune system and thus the effects of their products upon it.
Otherwise humanity might be in a bit of trouble.
Whatever happened to - It's what you don't know you don't know......
Yes that is clear, and you answered a question about my latest CBC. You didn't tell me anything I didn't already know about the CDC, but that's quite alright. Thank you!
Interesting, thanks. I was under the impression that humoral monocytes extravasate and become M1 or M2 macrophages with the M3 still a bit of an enigma in humans. Also never heard of monocyte/macrophage differentiation into DCs, although aware of DC subsets with DC-5 probably closest to a monocyte.
Cheers
I haven't looked too deeply into macrophage classification, but my impression is that they're more along a spectrum so there are some researchers that argue for abandoning M1/M2 nomenclature. https://www.ahajournals.org/doi/full/10.1161/CIRCRESAHA.116.309194
As for DC origins, here's how I understand it. For awhile both macrophages and DCs were thought to originate from monocytes. Then later some argued that macrophages and DCs derived independently from monocytes and originated from stem cells that were distinct from monocytes. BUT there's been some recent work suggesting that monocytes can also differentiate into DCs (or macrophages). More here on that: https://www.sciencedirect.com/science/article/abs/pii/S1084952117303622
Anyway, my guess is that there are some subsets of DCs that originate from stem cells distinct from monocytes, and some that are derived from monocytes ("mo-DCs" or monocyte-derived DCs). But our understanding of it is still evolving...
Hey Joomi, do you think it would be bad then, if, according to Pfizer's own study #185350, which the FDA tried to hide from the public for 75 years, the mRNA filled LNP's of the vaccine would end up in the bone marrow, detectable there 25 minutes after IM injection and rising in concentration until end of test at 48h after injection (starting at 0.489 accumulating to 3.771 μg lipid equiv/g (mL))? I mean do we want our hematopoietic stem cells to be swimming in a bath of LNPs all waiting to transfect them, producing spike protein only to be targeted then by our own immune system? Does anyone think that that would be a good thing?
btw, numbers taken from table 1 on page 23 of https://phmpt.org/wp-content/uploads/2022/03/125742_S1_M4_4223_185350.pdf
Oh, and one question: Has anyone seen any document describing which cell lines the LNP are NOT transfecting? Cause I have searched and so far it seems those LNPs are very UN-targeted.... so fi it its a neuron in your brain, a stem cell in your bone marrow, a cell in your spinal cord, or your heart muscle, the LNPs WILL transfect them, with the consequence being your immune system will kill those cells. So in short:
You got jab, you got brain damage.
I mean it's not impossible... I don't think it's something that's very likely given that HSCs make up such a tiny percentage of the cells in the bone marrow... but it's possible...
Fertig, et al. reported that peripheral blood mononuclear cells taking up LNPs tended not to produce any spike https://www.mdpi.com/2227-9059/10/7/1538
"However, of approximately 100 cells analysed, only three presented spikes, suggesting low levels of expression."
This could mean there are some cell types that do not express spike (perhaps due to post-translation processing differences that result in spike being scuttled) or that the vial they were testing was full of blanks or truncated RNAs. Anyone's guess.
If I understand it correctly, so far there have not been done any testing on what kind of cells will be able to be transfected (and again, I am pretty sure the LNPs do not differentiate between cell types) and then actually express the spike (this may be different though), though the study you quoted seems to suggest that this expression could be going on for as long as 60 days. And extracellular vesicles with spike on the outside were detected up to 4 months after injection! Here it would be very interesting to see, if those vesicles could lead to syncytia in tissue presenting ACE2... like the endothelial cell lining in every blood vessel in your body (vesicle could fuse with cell-> cell now presenting spike would fuse with neighbors presenting ACE2-> syncytia -> whatever problems would arise from syncytia of cells not normally seen to produce syncytia).
Great series. When will Part 4 be coming out? 🤔 Looking forward to it!