I can't say often enough how much I appreciate the absence of pearl-clutching in your writing.
The average citizen understands immunity only at the bumper sticker level (antibodies good!). Allopathic medicine's official stance is only marginally more detailed. Very few acknowledge that it's a complex system fraught with unintended consequences from tinkering.
Thank you - describing the immune system as our "biological self-destruct button" is a useful frame, strangely the phrase does not often appear in vaccine studies
Almost everyone in my personal life whom I care about is vaxxed and boosted. They are also almost all either obese or elderly. I am hoping that the significantly lessened effect of the mRNA vaxxes in the obese/elderly will make them less likely to end up with tolerance. In fact I am seeing old and fat vaxxed/boosted people doing pretty well; better than the young and skinny vaxxed/boosted people of my acquaintance. It would be ironic if my cousin in Indiana is saved by Cracker Barrel.
Couple of videos on the same topic by Dr. Mikolaj Raszek of Merogenomics, if anyone's interested. Not watched them yet, probably covers the same ground as Brian has but the more viewpoints the better:
IgG4 Antibodies part2 - why are they appearing? - update 87 IMPORTANT
The part 3 video is excellent. He outlines three reasons why the mRNA jabs may be inducing class switch. 1), and 2) are kind of obvious.. but number 3) is to my mind especially interesting and needs a deep dive...
1) Conc. of the antigen
2) Number of jabs sequentially
3) Type of vax, i.e. whole (killed) virus or sub-unit protein. There is some history of other such single protein jabs causing IgG4 class switch.
Regarding some of those, they are mentioned in the paper, but I didn't highlight them because the cited research doesn't clearly support the conclusions. E.g. with the pertussis example, the linked studies didn't clearly look at IgG4. Generally I'm not confident that IgG4 has been looked at with whole vaccines to any degree, which limits conclusions as far as subunit vaccines influencing IgG4. AFAIK the main work with whole/partial is Benn's overall mortality (non-specific effects) work, which is based on low-quality 3rd world record keeping.
Pretty astonishing that independent authors are having to do the thinking that apparently nobody in any regulatory authority worldwide did before allowing this mass experiment.
May 31, 2023·edited May 31, 2023Liked by Brian Mowrey
The tolerance effect could also be caused by contaminants. This person claims that the DNA plasmids contaminating the RNA shots can infect e coli in the gut and produce spike? Or maybe bare mRNA. I'm not sure how the production process works.
I'm pretty bearish on the plasmid contamination being a problem, as opposed to just a reflection of the lack of QA and external scrutiny of QA of the shots. All sorts of bacterial DNA is being shared by bacteria all the time, probably harmless to inject what is already everywhere. Meanwhile if LNPs can somehow transfect bacteria then that might not result in spike expression - I don't know if the compatibility of the UTRs chosen to optimize expression in human cells with bacteria has even been tested. And even some human cells seem not to express it.
May 31, 2023·edited May 31, 2023Liked by Brian Mowrey
Two things about this.. I think most bacterial DNA, like mRNA is eliminated intercellularly? So sneaking it in via LNP may be unexpected?
But the risk highlighted in that video was about transfecting into e coli. I thought that these plasmids are designed to work in e coli to produce the mRNA in the production process. So maybe it could turn gut bacteria into mRNA factories?
"Now some will argue that dsDNA and viral RNA is a false equivalency since the viral RNA is replication competent. This is false. The majority of the sgRNA you are detecting in a nasal swab in your nose is NOT REPLICATION COMPETENT as shown in Jaafar et al. It is just an RNA fragment that should have lower longevity in your cells than dsDNA contaminating fragments."
Thus, while the PCR tests may be accurate they might also be irrelevant.
I am not sure which post you are quoting. He references post-infection residual PCR positivity and makes a somewhat flippant claim that people were "quarantined" for CT<40 (who, when, where, it didn't happen. most people were PCR+'d when actually sick). Most places used 90 day moratoriums on reporting additional PCR+'s as additional cases. So reported cases based on PCR+ are virtually always relevant. If it takes you five minutes to dry and I see you are wet, as long as I don't count twice in a five minute period then I know that you being wet means you've gone in the water. That's relevance. So then one can say, "but I am not in the water ~now~." That hasn't diminished or altered the relevance of wetness, it's just sophistry.
Great article as usual. Looks like mainstream science establishment chooses to be rather superficial in it's understanding; the trademark claims of 'no evidence' really is a signal that evidence must not be sought, or at least any emerging evidence is actively ignored until forced to do otherwise.
Sorry if I’m being dense here, but why does tolerance to a specific antigen lead to an increased risk of cancer overall. I can understand it would mean possible increased susceptibility to the specific antigen in the future, and if that antigen was a marker on a cancer cell then I could see how the immune system could ignore it, but why would our immune system be out to kill us ( by ignoring cancers) just because we may have been overexposed to something?
IgG4 is believed to bind to the FC receptors on IgG1 that normally "tag" the things IgG1 attaches to for immune response from complement or cellular attack, and this isn't based on shared / cross-reactivity, it's just a generic nerfing of IgG1. If so, presumably it is not a big deal at normal IgG4 concentrations and there is a threshold when it interferes with normal IgG1 mediated function, but (presumably) this is not relevant in most scenarios since cancer introduces a persistent / chronic stimulus that predisposes to IgG4 conversion of the anti-cancer antibodies and other tolerance responses, in other words the shotgun FC-FC thing is less important than antigen-specific IgG4 "sniper" tolerance. But in the cited animal models it seems like the shotgun interference can be a risk at a high enough level of non-cancer-specific IgG4, so it's a possibility that can't be dismissed outright.
Highest risk windows for cancer growth would be subsequent to injection or during infection/subsequent to infection while IgG4 levels remain elevated? Basically, IgG4 binding to cancer cells expressing spike protein interferes with IgG1 binding?
The way I read it, IgG4 directly binds to the fc-receptor on Macrophages and T-cells, causing them to "relax" through some kind of chemical signaling. Leading to a general lowered immune system alertness wherever IgG4 antibodies are present.
Among immune ("effector") cell Fc receptors, IgG4 is ranked as competitive only for FcγRIIb
"because IgG4 has low affinity to activating FcγR while retaining relatively high affinity to the inhibiting FcγRIIb (Table (Table1),1), this may serve as an evolutionary way to prevent excessive immune responses against these sterile antigens not posing infectious threats. IgG4 has, therefore, been characterized as “blocking antibody,”" https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4202688/
I found the positioning of extra IgG4 in the cell receptors in Fig 3 to be inexplicable and redundant in the context of interfering with IgG1 anti-cancer antibodies. At all events the cited mouse models satisfied me that high non-specific IgG4 can be a generic theoretical cancer risk.
IgG4, as well as IgG2, both lack effector binding due to alterations to their Fc stalk, so they shouldn't be binding to receptors on effector cells. Keep in mind that one may argue that binding of effector cells to antibodies may lead to an overexaggerated immune response, and so shutting off this functionality may be done with the intent to shut down that over exaggerated response. So the alertness is intentionally stunted, but its by way of blocking effector cells from responding and becoming stimulated by antibodies.
In the little picture at the top of the article (which is taken from the paper), there appear to be free IgG4 antibodies binding to the Macrophage and the NK-cell's FC-receptors. Am I misinterpreting this picture? Are they supposed to only represent the IgG4 antibodies that are stuck to the anti-cancer IgG1s?
There also this sentence in the paper that I interpreted as a direct interaction between free IgG4 and immune cells: "It was discovered that IgG4 can contend with IgG1 (as shown in Figure 3) in binding to Fc receptors present in some immune cells in vitro."
It does appear to show that. The picture isn't wrong in its presentation (as in a cell labeled "macrophage" does appear to have an IgG4 antibody binding to it). However, this seems to go against what I've known to be how IgG4 works. The authors also comment that IgG4 also don't bind to antigens, which also doesn't appear to be accurate:
"The majority of IgG4 molecules will have two distinct Fab arms because of the half-antibody exchange, making them “bi-specific” and operationally univalent for a particular antigen. As a result, far from the other IgG subclasses, IgG4 antibodies in circulation are unable to form immunological complexes with antigens. IgG4 antibodies have a limited theoretical potential for immunological activation due to their weak affinity for C1q and Fc receptors."
So they're stating that immune complexes can't be formed between antigens, they state that there are weak affinities to Fc receptors, and yet they are showing binding of IgG4 to Fc receptors on effector cells.
This also seems to contradict this paragraph:
"IgG4′s reputation as a “blocking antibody” stems from its diminished capacity to elicit immune system effector reactions [43,44]. This implies that there will only be a minimal immune response when IgG4 interacts with molecules [45]. An IgG4 response can be either pathogenic or protective, depending on the situation. For instance, IgG4 is frequently referred to as a safeguarding blocking antibody because it can suppress or halt inflammation by competing with inflammatory IgE for antigen binding in the case of allergies and infections with helminth and filarial parasites. In contrast, IgG4 can lead to serious illness in several autoimmune disorders [46] as well as cancer [47,48]. Its bi-functionality will be thoroughly examined in the next subsections."
Which seems to argue that IgG4 competes for binding to antigens even though the reviewers are arguing that it shouldn't...
I would have to look at this review more close to make any judgement, but these paragraphs seem contradictory in my opinion.
May 31, 2023·edited May 31, 2023Liked by Brian Mowrey
I am somehow certain that this seldom cited 2009 paper had not escaped the attention of the COVID perpetrators, even if they did not engage with it reference-wise. I am quite disenchanted after seeing (from David Martin overview in EU parliament) how much of the harms of spike protein had been known so very well for so very long. All of those long known effects then packed into the injections. Plus now I learn there had also been a study from 2009 on IgG4. It turns out that over the centuries and decades, it becomes a real problem for societies when they do not have a mechanism in place like the Eskimos / Inuit seem to have. I forget the technical term but it's about eliminating sociopathy/psychopathy from the group gene pool.
I sort of felt like this review seemed redundant, but I think I just confused it for the review that was released a few months prior. I raised a point with respect to IgG4 an autoimmunity a while back as I just thought based on conjecture that seemed to have been a reactive, protective response from autoimmune responses. It's interesting that IgG4 doesn't appear to present in mice. I'm curious if this is an evolutionary consequence of longer life and a greater probability of being continuously exposed to an allergen/pathogen.
I think one point of contention I have with the IgG4 cancer argument is that if IgG4 is indiscriminate in the effector-ouroboros binding motif then shouldn't we expect higher incidences of cancer in relation to those with greater allergens? Or maybe that's something that hasn't been investigated due to lack of interest or lack of knowing.
The T-cell argument for autoimmunity seems interesting, although that seems like it would be easily answered by checking for cross-reactive responses. If the paratope of some antibodies diverts to target the host we shouldn't expect them to also cross-react, although that argument would have to be made in lieu of exposure to said cross-reactive antigen.
"I think one point of contention I have with the IgG4 cancer argument is that if IgG4 is indiscriminate in the effector-ouroboros binding motif then shouldn't we expect higher incidences of cancer in relation to those with greater allergens? Or maybe that's something that hasn't been investigated due to lack of interest or lack of knowing."
I asked myself this same question and followed this trail a bit... found one study of bee keepers that did not indicate a higher incidence of cancer.
I wasn't expecting the review to be as thought-provoking as it was; a good read.
Certainly post-allergy IgG4 could have a role / correlation to cancer that hasn't been investigated yet, since both seem to be post-industrial ailments.
Tsumiyama et al. seem to emphasize that their theory isn't about cross-reaction. It's just that over-stimulated T Cells go into "pollo loco mode" which observably promotes B Cell autoantibody proliferation. But I'm still processing the papers, including the one about sheep vaccines.
My remark with respect to Tsumiyama et al. was more towards the idea of easily falsifying their hypothesis. IF one were to argue that autoantibodies may be created in response to hyperactive T cells and constant antigen exposure, then conducting an assay where one takes some of those autoantibodies and seeing if they cross-react to the over-exposed antigen should refute that hypothesis.
I think we may just find that IgG4 may be a consequence of us living longer as well. IgG4 production in someone's 40s or 50s may make sense since prior times these people may not live much past those ages, but with an aging population maybe IgG4 levels may be seen along the same lines as dementia or other diseases of age. Just a curious thought.
I was hoping you’d take a look a look at it. I read Jessica’s excellent post and the review yesterday and immediately thought, “I wonder what Brian thinks.” Thanks for sharing your thoughts.
That's a strategically robust formulation of the virus/pandemic skepticism meme, so why should I rebut it? But as always it adds burdens when remembering that younger "we"s were totally fine, previously "anthraxed" "we"s were suddenly impervious to being "anthraxed" again, so hypothetical "anthraxers" are extremely bent on replicating anti-narrative aspects of virology (kids are fine, natural immunity is real) just to...? Flame 2022 Substack comment drama?
Not unlikely per se but complicated. You have to assume the head honchos want to disparage child non-risk, disparage natural immunity, to promote vaccines (as observable in the propaganda), but keep simulating evidence undercutting message (not anthraxing kids or previously sick), at a stratospheric logistical burden (who and where are kids / previously sick, avoid them). Whereas "it was a lab-made or natural coronavirus that adults lacked immunity for" totally explains kids+immunity=safe
“Despite offering an earth-shattering proposal to reshape how autoimmunity is understood to arise, with obvious and extreme implications for all vaccines, the 2009 paper only has 16 citations...”--This reaction isn’t surprising when one considers the power of the vaccine establishment, which is the money behind the status quo not only regarding vaccines, but great swaths of what passes for science today. The situation is firmly in line with Thomas Kuhn’s principles explained in “The Structure of Scientific Revolutions”.
May 31, 2023·edited May 31, 2023Liked by Brian Mowrey
The issue I am worried about is Fc-Fc binding.
Are IgG4 antibodies generated by the mRNA Gene Therapy only capable of binding to and neutralizing IgG1 antibodies generated by the mRNA Gene Therapy or are they able to neutralize all IgG1 antibodies?
Now, if Fc-Fc binding was non-specific you would expect IgG4 Abs against measles to neutralize other IgG1 Abs. However, with normal diseases like Measles maybe you never produce IgG4 Abs. So, maybe we are in uncharted territory.
Who knows. I suspect the 'experts' don't!
Another question is: How do IgG4 antibodies tell the rest of the immune system not to fuck with the thing they are attached to? Is it because the Fc portion encodes some sort of "Don't Fuck with me" signal or is it because it binds to the Fc portion of IgG1 antibodies and prevents other immune system effectors from binding?
Title "An immune evasion mechanism with IgG4 playing an essential role in cancer and implication for immunotherapy"
Quote from the paper "We further found that IgG4, regardless of its antigen specificity, inhibited the classic immune reactions of antibody-dependent cell-mediated cytotoxicity, antibody-dependent cellular phagocytosis and complement-dependent cytotoxicity against cancer cells in vitro, and these effects were obtained through its Fc fragment reacting to the Fc fragments of cancer-specific IgG1 that has been bound to cancer antigens. We also found that IgG4 competed with IgG1 in reacting to Fc receptors of immune effector cells."
IMO Brian is way too conservative in his approach to putting the pieces together. He wants 100% knowledge... meanwhile the fuckers are making mRNA flu shots for us.
It appears, then, that there are two distinct mechanisms for IgG4 Abs to cause tolerance and reduce the effect of IgG1 Abs:
1. IgG4 Abs have changes to their Fc regions (domains?) that prevent docking/binding to immune effector cells and they can prevent IgG1 Abs from binding to pathogens* by getting there first, and
2. Fc-Fc binding can neutralize IgG1 Abs already bound to a pathogen.
Have I got that right? Also, are IgG4 Abs non-specific when it comes to Fc-Fc binding? Will they neutralize any other IgG1 Abs?
* Here I also mean antigens from pathogens expressed on the surfaces of infected cells.
Since defense against viruses is a numbers game ... there must be a curve that shows the level of IgG4 that means your immune system becomes ineffective.
speaking of the "numbers" game view of IgG4 dominance... realizing that this work was done in macaques and not humans, look at the pie charts of post-booster IgG4 progression at the bottom of figure 1. Now do you see why the post-booster effect is not some anecdote?
OMG at those IgG4 levels. As for whether boosters are the story, would want to know week 17 (presumably before injection) draws. Conversion could already be at week 19 levels by then, we don't know. From supplemental it doesn't seem like they looked at IgG1/4 on weeks other than 6 and 19 so that's an important gap.
Added link. It doesn't seem like I can pin your comment since it is a reply. If you want to copy or rephrase the above in a standalone comment I will pin it, though.
I'm had forgotten that your post not only includes the doctor video I was thinking of with my vague reference to post-booster anecdotes, but emphasized the Fc-Fc mechanism - I will embed a link, wish I had remembered to begin with
It would appear that the Rat Juice injections ... are what will make this possible:
Dr. Lee Merritt explains how mRNA Vaccines killed animals during testing and how MRNA Vaccines could be used to kill millions of people by first injecting people with the So Called Vaccine and then releasing a counterpart even years later to be killed at will - She calls this a Binary Poison (as it's in two parts)
In a meeting of the World Health Assembly in Geneva, Switzerland, on Monday, director-general Dr. Tedros Adhanom Ghebreyesus sounded an alarm that the COVID-19 pandemic is far from over.
“The threat of another variant emerging that causes new surges of disease and death remains,” Tedros said. “And the threat of another pathogen emerging with even deadlier potential remains.”
The trigger for the release will be when the folks who run the world ... find themselves pushing on a string in terms of trying to prevent this bubble from exploding:
“I’m sitting here staring in the face at the biggest and probably the broadest asset bubble — forget that I’ve ever seen, but that I’ve ever studied,” Stanley Druckenmiller said at the May 2023 Sohn Investment Conference.
Overloading the immune system with antigens can cause class switching which from the looks of it can accelerate cancers and reduce virus clearance. Got it.
What if the mRNA mechanism of action lowers that threshold? Seems to me a logical conjecture since the DNA based vaccines didn’t show the switching phenomenon. It also kind of makes sense that it would take much less for the spike produced through mRNA to start to be recognized as “self” compared to DNA delivery through an adenovirus (delivery mechanism).
If that is correct, coupled with the fact that either 2 doses of mRNA or a higher dose is needed to produce a sufficient immune response, then mRNA as a platform has not only failed but will NEVER work as a vaccine platform.
What if... you knock down the immune systems of billions of people ... then you release a virus that is engineered to take advantage of this situation ... waltz past non-existent defences...
And kill the billions.
Then the remaining Unvaxxed (2 billion or so) starve to death.
May 31, 2023·edited May 31, 2023Liked by Brian Mowrey
Well, I remain convinced that the cancer wards saw too many people who were in remission suddenly get cancer again. I didn’t get any jabs and when I had cancer last year (one with pretty bad stats) I made sure to tell the lead oncologist that I was unvaccinated. I wanted her to make the connection. I am currently still in remission but you can tell that they are rather shocked by that. I somehow got in my chart that “I found the jab to be a possible p53 suppressant and therefore was reluctant to take it “ :) I’m kind of geeky proud that I got that in my chart.
Totally anecdotal, but my best friend is German and literally every person she knows (except her), has had 4 or more jabs. They are literally besieged by constant illness to the point where it is completely alarming, but they remain oblivious to any connection. 3 older family members died, one had cancer spread like wildfire, the other an aneurysm, another a sudden heart attack. The others sick, I mean literally its to the point that you can only count the days they felt well, and that is like 20% of the days since the first of January. We both mentioned that we are the only 2 sheep in that field that think the man and the dog are working together....
Excellent rundown of reality, Charlotte! The thing that’s missing in many investigative pieces is the acknowledgment that “anecdotal” is still empirical. It may not be “peer reviewed” or confirmed by double-blind studies to the liking of some writers--but with the state of studies and publications being what it is, I’ll take my chances with anecdotes over corruption and fake studies.
I can't say often enough how much I appreciate the absence of pearl-clutching in your writing.
The average citizen understands immunity only at the bumper sticker level (antibodies good!). Allopathic medicine's official stance is only marginally more detailed. Very few acknowledge that it's a complex system fraught with unintended consequences from tinkering.
Thank you - describing the immune system as our "biological self-destruct button" is a useful frame, strangely the phrase does not often appear in vaccine studies
Almost everyone in my personal life whom I care about is vaxxed and boosted. They are also almost all either obese or elderly. I am hoping that the significantly lessened effect of the mRNA vaxxes in the obese/elderly will make them less likely to end up with tolerance. In fact I am seeing old and fat vaxxed/boosted people doing pretty well; better than the young and skinny vaxxed/boosted people of my acquaintance. It would be ironic if my cousin in Indiana is saved by Cracker Barrel.
Couple of videos on the same topic by Dr. Mikolaj Raszek of Merogenomics, if anyone's interested. Not watched them yet, probably covers the same ground as Brian has but the more viewpoints the better:
IgG4 Antibodies part2 - why are they appearing? - update 87 IMPORTANT
https://www.youtube.com/watch?v=UT-kKlmEdEM
IgG4 part 3 - Proposed cause!
https://www.youtube.com/watch?v=yuehIrgOB9E
The part 3 video is excellent. He outlines three reasons why the mRNA jabs may be inducing class switch. 1), and 2) are kind of obvious.. but number 3) is to my mind especially interesting and needs a deep dive...
1) Conc. of the antigen
2) Number of jabs sequentially
3) Type of vax, i.e. whole (killed) virus or sub-unit protein. There is some history of other such single protein jabs causing IgG4 class switch.
Brian are you up for doing such a deep dive into single injected proteins? Hint: Class switch due to injected proteins is connected to IgE here; https://vinuarumugham.substack.com/p/long-before-eua-fda-and-vaccine-makers
Regarding some of those, they are mentioned in the paper, but I didn't highlight them because the cited research doesn't clearly support the conclusions. E.g. with the pertussis example, the linked studies didn't clearly look at IgG4. Generally I'm not confident that IgG4 has been looked at with whole vaccines to any degree, which limits conclusions as far as subunit vaccines influencing IgG4. AFAIK the main work with whole/partial is Benn's overall mortality (non-specific effects) work, which is based on low-quality 3rd world record keeping.
Thanks for highlighting, I haven't been keeping up on the youtube side. A good overview - lucky for him to get a sneak peak at the paper
It's been very interesting to watch his evolution over the last two years.
Thanks for a fascinating review.
Pretty astonishing that independent authors are having to do the thinking that apparently nobody in any regulatory authority worldwide did before allowing this mass experiment.
The mind boggles at the recklessness.
The tolerance effect could also be caused by contaminants. This person claims that the DNA plasmids contaminating the RNA shots can infect e coli in the gut and produce spike? Or maybe bare mRNA. I'm not sure how the production process works.
https://rense.com/general97/dna-plasmids.php
I'm pretty bearish on the plasmid contamination being a problem, as opposed to just a reflection of the lack of QA and external scrutiny of QA of the shots. All sorts of bacterial DNA is being shared by bacteria all the time, probably harmless to inject what is already everywhere. Meanwhile if LNPs can somehow transfect bacteria then that might not result in spike expression - I don't know if the compatibility of the UTRs chosen to optimize expression in human cells with bacteria has even been tested. And even some human cells seem not to express it.
Two things about this.. I think most bacterial DNA, like mRNA is eliminated intercellularly? So sneaking it in via LNP may be unexpected?
But the risk highlighted in that video was about transfecting into e coli. I thought that these plasmids are designed to work in e coli to produce the mRNA in the production process. So maybe it could turn gut bacteria into mRNA factories?
Eh, what could go wrong?
This substack seems to cover it quite well:
https://anandamide.substack.com/
Curiously, he says:
"Now some will argue that dsDNA and viral RNA is a false equivalency since the viral RNA is replication competent. This is false. The majority of the sgRNA you are detecting in a nasal swab in your nose is NOT REPLICATION COMPETENT as shown in Jaafar et al. It is just an RNA fragment that should have lower longevity in your cells than dsDNA contaminating fragments."
Thus, while the PCR tests may be accurate they might also be irrelevant.
I am not sure which post you are quoting. He references post-infection residual PCR positivity and makes a somewhat flippant claim that people were "quarantined" for CT<40 (who, when, where, it didn't happen. most people were PCR+'d when actually sick). Most places used 90 day moratoriums on reporting additional PCR+'s as additional cases. So reported cases based on PCR+ are virtually always relevant. If it takes you five minutes to dry and I see you are wet, as long as I don't count twice in a five minute period then I know that you being wet means you've gone in the water. That's relevance. So then one can say, "but I am not in the water ~now~." That hasn't diminished or altered the relevance of wetness, it's just sophistry.
Great article as usual. Looks like mainstream science establishment chooses to be rather superficial in it's understanding; the trademark claims of 'no evidence' really is a signal that evidence must not be sought, or at least any emerging evidence is actively ignored until forced to do otherwise.
Sorry if I’m being dense here, but why does tolerance to a specific antigen lead to an increased risk of cancer overall. I can understand it would mean possible increased susceptibility to the specific antigen in the future, and if that antigen was a marker on a cancer cell then I could see how the immune system could ignore it, but why would our immune system be out to kill us ( by ignoring cancers) just because we may have been overexposed to something?
IgG4 is believed to bind to the FC receptors on IgG1 that normally "tag" the things IgG1 attaches to for immune response from complement or cellular attack, and this isn't based on shared / cross-reactivity, it's just a generic nerfing of IgG1. If so, presumably it is not a big deal at normal IgG4 concentrations and there is a threshold when it interferes with normal IgG1 mediated function, but (presumably) this is not relevant in most scenarios since cancer introduces a persistent / chronic stimulus that predisposes to IgG4 conversion of the anti-cancer antibodies and other tolerance responses, in other words the shotgun FC-FC thing is less important than antigen-specific IgG4 "sniper" tolerance. But in the cited animal models it seems like the shotgun interference can be a risk at a high enough level of non-cancer-specific IgG4, so it's a possibility that can't be dismissed outright.
Highest risk windows for cancer growth would be subsequent to injection or during infection/subsequent to infection while IgG4 levels remain elevated? Basically, IgG4 binding to cancer cells expressing spike protein interferes with IgG1 binding?
The way I read it, IgG4 directly binds to the fc-receptor on Macrophages and T-cells, causing them to "relax" through some kind of chemical signaling. Leading to a general lowered immune system alertness wherever IgG4 antibodies are present.
Did I get this totally wrong?
Among immune ("effector") cell Fc receptors, IgG4 is ranked as competitive only for FcγRIIb
"because IgG4 has low affinity to activating FcγR while retaining relatively high affinity to the inhibiting FcγRIIb (Table (Table1),1), this may serve as an evolutionary way to prevent excessive immune responses against these sterile antigens not posing infectious threats. IgG4 has, therefore, been characterized as “blocking antibody,”" https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4202688/
I found the positioning of extra IgG4 in the cell receptors in Fig 3 to be inexplicable and redundant in the context of interfering with IgG1 anti-cancer antibodies. At all events the cited mouse models satisfied me that high non-specific IgG4 can be a generic theoretical cancer risk.
Thanks, that's a clarifying answer.
IgG4, as well as IgG2, both lack effector binding due to alterations to their Fc stalk, so they shouldn't be binding to receptors on effector cells. Keep in mind that one may argue that binding of effector cells to antibodies may lead to an overexaggerated immune response, and so shutting off this functionality may be done with the intent to shut down that over exaggerated response. So the alertness is intentionally stunted, but its by way of blocking effector cells from responding and becoming stimulated by antibodies.
In the little picture at the top of the article (which is taken from the paper), there appear to be free IgG4 antibodies binding to the Macrophage and the NK-cell's FC-receptors. Am I misinterpreting this picture? Are they supposed to only represent the IgG4 antibodies that are stuck to the anti-cancer IgG1s?
There also this sentence in the paper that I interpreted as a direct interaction between free IgG4 and immune cells: "It was discovered that IgG4 can contend with IgG1 (as shown in Figure 3) in binding to Fc receptors present in some immune cells in vitro."
It does appear to show that. The picture isn't wrong in its presentation (as in a cell labeled "macrophage" does appear to have an IgG4 antibody binding to it). However, this seems to go against what I've known to be how IgG4 works. The authors also comment that IgG4 also don't bind to antigens, which also doesn't appear to be accurate:
"The majority of IgG4 molecules will have two distinct Fab arms because of the half-antibody exchange, making them “bi-specific” and operationally univalent for a particular antigen. As a result, far from the other IgG subclasses, IgG4 antibodies in circulation are unable to form immunological complexes with antigens. IgG4 antibodies have a limited theoretical potential for immunological activation due to their weak affinity for C1q and Fc receptors."
So they're stating that immune complexes can't be formed between antigens, they state that there are weak affinities to Fc receptors, and yet they are showing binding of IgG4 to Fc receptors on effector cells.
This also seems to contradict this paragraph:
"IgG4′s reputation as a “blocking antibody” stems from its diminished capacity to elicit immune system effector reactions [43,44]. This implies that there will only be a minimal immune response when IgG4 interacts with molecules [45]. An IgG4 response can be either pathogenic or protective, depending on the situation. For instance, IgG4 is frequently referred to as a safeguarding blocking antibody because it can suppress or halt inflammation by competing with inflammatory IgE for antigen binding in the case of allergies and infections with helminth and filarial parasites. In contrast, IgG4 can lead to serious illness in several autoimmune disorders [46] as well as cancer [47,48]. Its bi-functionality will be thoroughly examined in the next subsections."
Which seems to argue that IgG4 competes for binding to antigens even though the reviewers are arguing that it shouldn't...
I would have to look at this review more close to make any judgement, but these paragraphs seem contradictory in my opinion.
I am somehow certain that this seldom cited 2009 paper had not escaped the attention of the COVID perpetrators, even if they did not engage with it reference-wise. I am quite disenchanted after seeing (from David Martin overview in EU parliament) how much of the harms of spike protein had been known so very well for so very long. All of those long known effects then packed into the injections. Plus now I learn there had also been a study from 2009 on IgG4. It turns out that over the centuries and decades, it becomes a real problem for societies when they do not have a mechanism in place like the Eskimos / Inuit seem to have. I forget the technical term but it's about eliminating sociopathy/psychopathy from the group gene pool.
I think the technical term might be “kunlangeta”.
Exactly! Only Kuomintang came to mind ...
I sort of felt like this review seemed redundant, but I think I just confused it for the review that was released a few months prior. I raised a point with respect to IgG4 an autoimmunity a while back as I just thought based on conjecture that seemed to have been a reactive, protective response from autoimmune responses. It's interesting that IgG4 doesn't appear to present in mice. I'm curious if this is an evolutionary consequence of longer life and a greater probability of being continuously exposed to an allergen/pathogen.
I think one point of contention I have with the IgG4 cancer argument is that if IgG4 is indiscriminate in the effector-ouroboros binding motif then shouldn't we expect higher incidences of cancer in relation to those with greater allergens? Or maybe that's something that hasn't been investigated due to lack of interest or lack of knowing.
The T-cell argument for autoimmunity seems interesting, although that seems like it would be easily answered by checking for cross-reactive responses. If the paratope of some antibodies diverts to target the host we shouldn't expect them to also cross-react, although that argument would have to be made in lieu of exposure to said cross-reactive antigen.
"I think one point of contention I have with the IgG4 cancer argument is that if IgG4 is indiscriminate in the effector-ouroboros binding motif then shouldn't we expect higher incidences of cancer in relation to those with greater allergens? Or maybe that's something that hasn't been investigated due to lack of interest or lack of knowing."
I asked myself this same question and followed this trail a bit... found one study of bee keepers that did not indicate a higher incidence of cancer.
I wasn't expecting the review to be as thought-provoking as it was; a good read.
Certainly post-allergy IgG4 could have a role / correlation to cancer that hasn't been investigated yet, since both seem to be post-industrial ailments.
Tsumiyama et al. seem to emphasize that their theory isn't about cross-reaction. It's just that over-stimulated T Cells go into "pollo loco mode" which observably promotes B Cell autoantibody proliferation. But I'm still processing the papers, including the one about sheep vaccines.
My remark with respect to Tsumiyama et al. was more towards the idea of easily falsifying their hypothesis. IF one were to argue that autoantibodies may be created in response to hyperactive T cells and constant antigen exposure, then conducting an assay where one takes some of those autoantibodies and seeing if they cross-react to the over-exposed antigen should refute that hypothesis.
I think we may just find that IgG4 may be a consequence of us living longer as well. IgG4 production in someone's 40s or 50s may make sense since prior times these people may not live much past those ages, but with an aging population maybe IgG4 levels may be seen along the same lines as dementia or other diseases of age. Just a curious thought.
I was hoping you’d take a look a look at it. I read Jessica’s excellent post and the review yesterday and immediately thought, “I wonder what Brian thinks.” Thanks for sharing your thoughts.
Mowrey, is it possible that we all got Anthraxed?
With a predetermined coronavirus sequence inserted to appease the pretermined PCR test sequence?
That's a strategically robust formulation of the virus/pandemic skepticism meme, so why should I rebut it? But as always it adds burdens when remembering that younger "we"s were totally fine, previously "anthraxed" "we"s were suddenly impervious to being "anthraxed" again, so hypothetical "anthraxers" are extremely bent on replicating anti-narrative aspects of virology (kids are fine, natural immunity is real) just to...? Flame 2022 Substack comment drama?
I *think that was a "yes it is possible, but unlikely"?
Not unlikely per se but complicated. You have to assume the head honchos want to disparage child non-risk, disparage natural immunity, to promote vaccines (as observable in the propaganda), but keep simulating evidence undercutting message (not anthraxing kids or previously sick), at a stratospheric logistical burden (who and where are kids / previously sick, avoid them). Whereas "it was a lab-made or natural coronavirus that adults lacked immunity for" totally explains kids+immunity=safe
“Despite offering an earth-shattering proposal to reshape how autoimmunity is understood to arise, with obvious and extreme implications for all vaccines, the 2009 paper only has 16 citations...”--This reaction isn’t surprising when one considers the power of the vaccine establishment, which is the money behind the status quo not only regarding vaccines, but great swaths of what passes for science today. The situation is firmly in line with Thomas Kuhn’s principles explained in “The Structure of Scientific Revolutions”.
The issue I am worried about is Fc-Fc binding.
Are IgG4 antibodies generated by the mRNA Gene Therapy only capable of binding to and neutralizing IgG1 antibodies generated by the mRNA Gene Therapy or are they able to neutralize all IgG1 antibodies?
Now, if Fc-Fc binding was non-specific you would expect IgG4 Abs against measles to neutralize other IgG1 Abs. However, with normal diseases like Measles maybe you never produce IgG4 Abs. So, maybe we are in uncharted territory.
Who knows. I suspect the 'experts' don't!
Another question is: How do IgG4 antibodies tell the rest of the immune system not to fuck with the thing they are attached to? Is it because the Fc portion encodes some sort of "Don't Fuck with me" signal or is it because it binds to the Fc portion of IgG1 antibodies and prevents other immune system effectors from binding?
There is evidence for the Fc-Fc binding - I highlighted it here; https://lettingdataspeak.substack.com/p/tying-together-the-elements-of-an
Here is the paper itself;
https://jitc.bmj.com/content/8/2/e000661
Title "An immune evasion mechanism with IgG4 playing an essential role in cancer and implication for immunotherapy"
Quote from the paper "We further found that IgG4, regardless of its antigen specificity, inhibited the classic immune reactions of antibody-dependent cell-mediated cytotoxicity, antibody-dependent cellular phagocytosis and complement-dependent cytotoxicity against cancer cells in vitro, and these effects were obtained through its Fc fragment reacting to the Fc fragments of cancer-specific IgG1 that has been bound to cancer antigens. We also found that IgG4 competed with IgG1 in reacting to Fc receptors of immune effector cells."
IMO Brian is way too conservative in his approach to putting the pieces together. He wants 100% knowledge... meanwhile the fuckers are making mRNA flu shots for us.
Wait. In the piece you cite from Wang et al (https://jitc.bmj.com/content/8/2/e000661) it says:
"We also found that IgG4 competed with IgG1 in reacting to Fc receptors of immune effector cells."
But others have stated that the IgG4 Fc region cannot bind to effector cells.
Now I am confused.
It appears, then, that there are two distinct mechanisms for IgG4 Abs to cause tolerance and reduce the effect of IgG1 Abs:
1. IgG4 Abs have changes to their Fc regions (domains?) that prevent docking/binding to immune effector cells and they can prevent IgG1 Abs from binding to pathogens* by getting there first, and
2. Fc-Fc binding can neutralize IgG1 Abs already bound to a pathogen.
Have I got that right? Also, are IgG4 Abs non-specific when it comes to Fc-Fc binding? Will they neutralize any other IgG1 Abs?
* Here I also mean antigens from pathogens expressed on the surfaces of infected cells.
Since defense against viruses is a numbers game ... there must be a curve that shows the level of IgG4 that means your immune system becomes ineffective.
speaking of the "numbers" game view of IgG4 dominance... realizing that this work was done in macaques and not humans, look at the pie charts of post-booster IgG4 progression at the bottom of figure 1. Now do you see why the post-booster effect is not some anecdote?
https://www.science.org/doi/10.1126/sciimmunol.adg7015
OMG at those IgG4 levels. As for whether boosters are the story, would want to know week 17 (presumably before injection) draws. Conversion could already be at week 19 levels by then, we don't know. From supplemental it doesn't seem like they looked at IgG1/4 on weeks other than 6 and 19 so that's an important gap.
Agreed.. in this study the IgG4 data was kind of an afterthought... but very interesting to say the least.
Added link. It doesn't seem like I can pin your comment since it is a reply. If you want to copy or rephrase the above in a standalone comment I will pin it, though.
I'm had forgotten that your post not only includes the doctor video I was thinking of with my vague reference to post-booster anecdotes, but emphasized the Fc-Fc mechanism - I will embed a link, wish I had remembered to begin with
"However, since mRNA appear to vaccine induce IgG4 due to the ..."
Seems like words got out of order here.
Thanks! - missing words
It would appear that the Rat Juice injections ... are what will make this possible:
Dr. Lee Merritt explains how mRNA Vaccines killed animals during testing and how MRNA Vaccines could be used to kill millions of people by first injecting people with the So Called Vaccine and then releasing a counterpart even years later to be killed at will - She calls this a Binary Poison (as it's in two parts)
https://humansarefree.com/2021/01/dr-lee-merritt-animal-studies-mrna-technology-all-animals-died.html
In a meeting of the World Health Assembly in Geneva, Switzerland, on Monday, director-general Dr. Tedros Adhanom Ghebreyesus sounded an alarm that the COVID-19 pandemic is far from over.
“The threat of another variant emerging that causes new surges of disease and death remains,” Tedros said. “And the threat of another pathogen emerging with even deadlier potential remains.”
https://www.news.com.au/world/coronavirus/the-next-pandemic-even-deadlier-than-covid-is-coming-warns-who/news-story/20be6a458bf55b01143d752b2b0fa1d6
The trigger for the release will be when the folks who run the world ... find themselves pushing on a string in terms of trying to prevent this bubble from exploding:
“I’m sitting here staring in the face at the biggest and probably the broadest asset bubble — forget that I’ve ever seen, but that I’ve ever studied,” Stanley Druckenmiller said at the May 2023 Sohn Investment Conference.
Overloading the immune system with antigens can cause class switching which from the looks of it can accelerate cancers and reduce virus clearance. Got it.
What if the mRNA mechanism of action lowers that threshold? Seems to me a logical conjecture since the DNA based vaccines didn’t show the switching phenomenon. It also kind of makes sense that it would take much less for the spike produced through mRNA to start to be recognized as “self” compared to DNA delivery through an adenovirus (delivery mechanism).
If that is correct, coupled with the fact that either 2 doses of mRNA or a higher dose is needed to produce a sufficient immune response, then mRNA as a platform has not only failed but will NEVER work as a vaccine platform.
What if... you knock down the immune systems of billions of people ... then you release a virus that is engineered to take advantage of this situation ... waltz past non-existent defences...
And kill the billions.
Then the remaining Unvaxxed (2 billion or so) starve to death.
What if....
Just a thought...
If it is too virulent it won't spread. But something that becomes chronic through tolerance and slowly destroys the body.. may already exist in sars2.
One thing I just realized is the j&j shot that doesn't produce tolerance was quickly taken off the market. Perhaps that was the reason.
Well, I remain convinced that the cancer wards saw too many people who were in remission suddenly get cancer again. I didn’t get any jabs and when I had cancer last year (one with pretty bad stats) I made sure to tell the lead oncologist that I was unvaccinated. I wanted her to make the connection. I am currently still in remission but you can tell that they are rather shocked by that. I somehow got in my chart that “I found the jab to be a possible p53 suppressant and therefore was reluctant to take it “ :) I’m kind of geeky proud that I got that in my chart.
Totally anecdotal, but my best friend is German and literally every person she knows (except her), has had 4 or more jabs. They are literally besieged by constant illness to the point where it is completely alarming, but they remain oblivious to any connection. 3 older family members died, one had cancer spread like wildfire, the other an aneurysm, another a sudden heart attack. The others sick, I mean literally its to the point that you can only count the days they felt well, and that is like 20% of the days since the first of January. We both mentioned that we are the only 2 sheep in that field that think the man and the dog are working together....
Excellent rundown of reality, Charlotte! The thing that’s missing in many investigative pieces is the acknowledgment that “anecdotal” is still empirical. It may not be “peer reviewed” or confirmed by double-blind studies to the liking of some writers--but with the state of studies and publications being what it is, I’ll take my chances with anecdotes over corruption and fake studies.