Memory T CELLS COVID 19

Drareg

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I’m starting this thread to add to as more develops on memory T Cells in relation to covid19. The idiots are trying to justify mass tracking and immunity passports based solely on antibodies when we should now be testing for T cells.
We all have living experience of COVID19’s exaggerated virulence being used to justify tyrant like legislation, it’s being used as an excuse via to bailout banks, big corporate groups, cover an elite paedo ring a la Epstein and provide a tax payer funded lotto to big pharma.

Unfortunately there are many who have been indoctrinated into a cult, their cult leaders made said cult members bailout banks in 2008 and are basically giving the 1% free money again in 2019/20, the cult members still "trust" their cult leaders so much the leaders no longer even have to use science to justify anything, they are basically just pathologically lying and are believed.

With the above in mind it’s good to start getting familiar with T cells because the ruling class are pumping dodgy Chinese antibody tests with false positives and false negatives, these dodgy antibody tests will be used for dodgy immunity passports. Many of us may have T Cells which means the ruling class won’t like this and T cells may go the way of Sweden, the country who
may never be named in any covid MSM debate again
.:beammeup

Remember your government care about you, it’s all for you, they can absolutely be trusted! Don’t look at recent historic facts to verify this, have faith, just believe because it feels good.
#we’re all in this together #the gulag together forever.

The article below is from a big pharma shill outlet, they see the research and think about Vaccines, they are pathological ,humans are basically moving dollar symbols, still it covers what T cells are doing here.
Immune T Cells May Offer Lasting Protection Against COVID-19

"Much of the study on the immune response to SARS-CoV-2, the novel coronavirus that causes COVID-19, has focused on the production of antibodies. But, in fact, immune cells known as memory T cells also play an important role in the ability of our immune systems to protect us against many viral infections, including—it now appears—COVID-19".

"An intriguing new study of these memory T cells suggests they might protect some people newly infected with SARS-CoV-2 by remembering past encounters with other human coronaviruses. This might potentially explain why some people seem to fend off the virus and may be less susceptible to becoming severely ill with COVID-19"


"SARS-CoV-2 belongs to a large family of coronaviruses, six of which were previously known to infect humans. Four of them are responsible for the common cold. The other two are more dangerous: SARS-CoV-1, the virus responsible for the outbreak of Severe Acute Respiratory Syndrome (SARS), which ended in 2004; and MERS-CoV, the virus that causes Middle East Respiratory Syndrome (MERS), first identified in Saudi Arabia in 2012.

All six previously known coronaviruses spark production of both antibodies and memory T cells. In addition, studies of immunity to SARS-CoV-1 have shown that T cells stick around for many years longer than acquired antibodies. So, Bertoletti’s team set out to gain a better understanding of T cell immunity against the novel coronavirus".


"The researchers gathered blood samples from 36 people who’d recently recovered from mild to severe COVID-19. They focused their attention on T cells (including CD4 helper and CD8 cytotoxic, both of which can function as memory T cells). They identified T cells that respond to the SARS-CoV-2 nucleocapsid, which is a structural protein inside the virus. They also detected T cell responses to two non-structural proteins that SARS-CoV-2 needs to make additional copies of its genome and spread. The team found that all those recently recovered from COVID-19 produced T cells that recognize multiple parts of SARS-CoV-2.

Next, they looked at blood samples from 23 people who’d survived SARS. Their studies showed that those individuals still had lasting memory T cells today, 17 years after the outbreak. Those memory T cells, acquired in response to SARS-CoV-1, also recognized parts of SARS-CoV-2.

Finally, Bertoletti’s team looked for such T cells in blood samples from 37 healthy individuals with no history of either COVID-19 or SARS. To their surprise, more than half had T cells that recognize one or more of the SARS-CoV-2 proteins under study here. It’s still not clear if this acquired immunity stems from previous infection with coronaviruses that cause the common cold or perhaps from exposure to other as-yet unknown coronaviruses".

The actual study is here -SARS-CoV-2-specific T cell immunity in cases of COVID-19 and SARS, and uninfected controls | Nature

"Memory T cells induced by previous pathogens can shape the susceptibility to, and clinical severity of, subsequent infections1. Little is known about the presence of pre-existing memory T cells in humans with the potential to recognize SARS-CoV-2. Here, we first studied T cell responses to structural (nucleocapsid protein, NP) and non-structural (NSP-7 and NSP13 of ORF1) regions of SARS-CoV-2 in COVID-19 convalescents (n=36). In all of them we demonstrated the presence of CD4 and CD8 T cells recognizing multiple regions of the NP protein. We then showed that SARS-recovered patients (n=23) still possess long-lasting memory T cells reactive to SARS-NP 17 years after the 2003 outbreak, which displayed robust cross-reactivity to SARS-CoV-2 NP. Surprisingly, we also frequently detected SARS-CoV-2 specific T cells in individuals with no history of SARS, COVID-19 or contact with SARS/COVID-19 patients (n=37). SARS-CoV-2 T cells in uninfected donors exhibited a different pattern of immunodominance, frequently targeting the ORF-1-coded proteins NSP7 and 13 as well as the NP structural protein. Epitope characterization of NSP7-specific T cells showed recognition of protein fragments with low homology to “common cold” human coronaviruses but conserved amongst animal betacoranaviruses. Thus, infection with betacoronaviruses induces multispecific and long-lasting T cell immunity to the structural protein NP. Understanding how pre-existing NP- and ORF-1-specific T cells present in the general population impact susceptibility and pathogenesis of SARS-CoV-2 infection is of paramount importance for the management of the current COVID-19 pandemic".
 

yerrag

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Good thread.

I'd like to share this Youtube playlist: Biology - Immune System - YouTube

AK Lectures does a fantastic job explaining the immune system. I highly recommend listening to all of it. I did that and it helped me understand the many terms and concepts discussed in readings on immunity. Without such understanding, many of what is discussed in the earlier post by Drareg would just go over my head. But if we are really to understand the issues talked about in relation to COVID-19, we have to appreciate the inner working of our immune system.

After going through this, for example, I can very well appreciate how much it is for us to take care of our thymus gland, as this is where immmature T-cells made by the bone marrow goes to become mature. Ray Peat had talked about having chronically high levels of cortisol being detrimental to the health of the thymus gland. Knowing this, I can see how important it is for us to have low cortisol levels, and one way to achieve that is to have stable blood sugar levels.

Anyway, hope people can find the youtube playlist helpful in gaining a better understanding of our immune system. Know this, and the less you will rely on WHO and CDC proclamations that push drugs and vaccines to us. And you will understand why it is not in best interest to follow these Pied Pipers.
 

lvysaur

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With the above in mind it’s good to start getting familiar with T cells because the ruling class are pumping dodgy Chinese antibody tests with false positives and false negatives
Why blame China when the most popular antibody test is created by Roche, a Western company?
 
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Drareg

Drareg

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Why blame China when the most popular antibody test is created by Roche, a Western company?

Sarcasm, when it’s found to be a failure they will pin it on China.
 
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Drareg

Drareg

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I will add another article from a pro covid journalist who seems to be starting to see the light-
Why your negative antibody test might be wrong - UnHerd

"There’s a bigger picture here, which is that if lots of people have the disease and then test negative, it changes our understanding of how widely the disease has spread in the population. Back in early July there were some shocking papers that came out, notably one from Spain which despite an awful outbreak found that only 5% of the population had a positive antibody response. It really set the scale of the problem into perspective, and how far from herd immunity we were.

These KCL findings — if they’re confirmed, I should say, because it’s still a relatively small study and because the sample might not be entirely representative — might shift that somewhat. Spector and Steves say that it could be that serology tests miss up to 50% of real cases. If that’s true, then up to about 10% of Spanish people may have had the disease — and perhaps more relevantly to most readers of this, up to 12% of British people, double the 6% estimate from the ONS. That’s an upper bound, and “it’s probably more likely in the middle”, says Steves. So it’s good news, but only cautiously so; it doesn’t give much support to wilder ideas that half of the population will have had it. Spector still puts the infection fatality rate at around 1%".
 
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Drareg

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Drareg

Drareg

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Another article on T cells, it’s interesting that a virus comes out of nowhere that doesn’t create antibodies in everyone, it bypasses the initial system response in some.
This is an interesting question for Peat, how can we boost T cells before a test?
Do they know the T cells being elevated are specific for covid 19 ,will the test be that accurate?
This may be a way to bypass bill epstein gates impotence vaccine.https://www.nationalgeographic.com/...dies-not-only-key-to-beating-coronavirus-cvd/

https://www.nationalgeographic.com/...dies-not-only-key-to-beating-coronavirus-cvd/
Why antibodies may not be the key to beating coronavirus


"The body should produce both protective antibodies, which keep the virus from invading, and killer T cells, which tell virus-infected human cells to destroy themselves to keep the virus from spreading. Normally, these immune responses appear in tandem. But in a subset of those who tested positive for COVID-19, Aleman found T cells but no antibodies.
Other scientists around the world also had similar findings. Much of this work is still preliminary, and scientists don’t know what it means in terms of assessing how well a vaccine will work or how well people are protected from severe forms of the disease. But one thing is becoming clear: antibodies might not be telling the whole story when it comes to COVID-19 immunity. “We shouldn’t just look blindly at antibody tests,” Aleman says"


Wellness gurus may exhort us to treat our bodies like temples, but when it comes to fighting off pathogens, the body is more like a castle under siege. Like any fortress, the body has several lines of defenses to protect it from infectious microbes.

The innate immune system is the first line, and it sets out to discourage any potential intruder by making the body as inhospitable for them as possible by raising the body’s temperature with a fever and assaulting pathogens with toxic chemicals. It acts like an overzealous security guard and reacts against any sign that a cell or protein is not the body’s own.

Even these security forces can be overwhelmed and outmaneuvered by pathogens that have evolved stealth to evade the immune system and counter inflammatory responses dedicated to stopping germs. When that happens, the adaptive immune system kicks in—and that’s when we see things like antibodies and T cells. These defenses emerge after a pathogen has invaded, and the body has learned the type of threat it poses.

B cells produce antibodies, small proteins that recognize certain pieces of a pathogen known as epitopes. If enough antibodies bind to a virus, it can’t enter the body’s cells to make copies of itself, and thus cannot make you sick. Likewise, killer T cells recognize epitopes displayed by virus-infected cells and tell the cells to self-destruct.

It's a process that has evolved over hundreds of millions of years, and all the different arms of the immune system generally work together seamlessly


Historically during epidemics, scientists have focused on antibody responses rather than T cells, because antibodies are easier to measure in the lab. Antibodies can be detected directly from a blood sample, explains Daniela Weiskopf, an immunologist at the La Jolla Institute for Immunology in California.

When Weiskopf wants to spot a T cell response, however, she has to reenact the series of steps the T cells use to identify a pathogen. First, she synthesizes a library of all the possible tiny epitopes the T cells can recognize. Then she needs to isolate the T cells from the blood and test them against all the different protein epitopes, to see which ones interact with the cells.

For most viruses, antibody and T cell responses usually match up in terms of timing and strength of response, so scientists generally rely on antibody tests alone because they are quicker, cheaper, and easier to administer. Some antibody test kits can provide results in minutes to hours, whereas T cell tests need to be sent to a specialized lab.

“It’s just not practical to test for T cell response in large samples,” says Weiskopf.

It was very strange and very surprising,” Aleman says. The study results, released June 29 without peer review via the medical pre-print service medRxiv, didn’t reveal whether these individuals never developed antibodies or whether they rapidly declined to undetectable levels. Regardless, the report immediately raised concerns about a vaccine, since stimulating antibody production is a key strategy by which immunizations protect against disease.

This apparent decline in antibodies was reported again on July 21, in 34 individuals with mild COVID-19 infections. If some people infected with SARS-CoV-2 don’t produce antibodies, it could mean they might not respond to a vaccine.


SARS-CoV-2 is one of seven known coronaviruses that can infect humans. The original SARS virus vanished after creating large outbreaks in 2003, and the Middle Eastern Respiratory Syndrome (MERS) virus has only infected a small number of people in the Middle East and North Africa. Four other coronaviruses circulate widely and cause the common cold.

Immunity to the common cold coronaviruses only lasts a year or two, which is why sniffles and stuffiness remain a pervasive part of life. However, patients infected with the original SARS virus still possessed memory T cells that responded to the virus’ proteins 17 years later, immunologist Antonio Bertoletti at Duke-NUS Medical School in Singapore recently reported in Nature. These same memory T cells also reacted to SARS-CoV-2. It’s something Bertoletti says bodes well for COVID-19.

 

yerrag

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This is an interesting question for Peat, how can we boost T cells before a test?
He says cortisol makes the thymus smaller. The implication, as Peat leaves us to find out why, is that cortisol decreases T-cell production, as it is in the thymus gland that T-cells mature. The immature T-cells are produced in the bone marrow.

My take then is that good sugar regulation is very important to T-cell health. With good sugar regulation, there is hardly a need to produce cortisol.
 
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Drareg

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It’s also interesting if this virus was not simulating antibodies for vaccine creation, I mean millions of people would be showing no antibodies even those infected justifying their vaccine for the masses, all they had to do was stimulate antibodies with the vaccine and claim they are covid antibodies when in reality we needed T cells.The antibodies don’t seem to stick around either probably why bill Epstein gates was saying we need multiple shots.
I’m veering into conspiracy but I think it’s important to engage the potentialities when we look at the current non scientific behavior being pumped by so called experts.
 
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Drareg

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He says cortisol makes the thymus smaller. The implication, as Pest leaves us to find out why, is that cortisol decreases T-cell production, as it is in the thymus gland that T-cells mature. The immature T-cells are. produced in the bone marrow.

My take then is that good sugar regulation is very important to T-cell health. With good sugar regulation, there is hardly a need to produce cortisol.

Was this in his recent interview? Danny Roddy is interviewing him again soon so maybe he will be more specific.

This could also explain why more males are dying, research being done on progesterone relative to covid19 makes sense, progesterone does have specific action on cortisol "receptors".
Another interesting pattern I see in covid19 recovery group is the claim it’s like chronic fatigue syndrome, the thing is many of them claim they were perfectly healthy, if you look into it you find it’s full of long distance runners, tri-fit types, triathlons and the like. This lot basically run on cortisol after years of doing that, many are over 30 and doing excessive exercise for years and don’t have the same recovery as they had in their 20’s with regard to protective hormones.
 

yerrag

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I heard this recently in one interview with Patrick Timpone, at the time when we were at the height of COVID threading and posting, going as far back as April.

I think this forum needs to understand this well. Many like to talk SFA but don't walk the talk. No one goes on a 4yr PUFA cold turkey intervention. Most would rather settle for aspirin and niacinamide, and a lot of other supplements. They can dispense with all that after going through true PUFA depletion.

It sets a good foundation for more improvements with blood sugar regulation. When that is achieved, cortisol is no longer an issue. And with little cortisol, thymus health gets better. And your immunity takes a leap.
 

lvysaur

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I heard this recently in one interview with Patrick Timpone, at the time when we were at the height of COVID threading and posting, going as far back as April.

I think this forum needs to understand this well. Many like to talk SFA but don't walk the talk. No one goes on a 4yr PUFA cold turkey intervention.
What are you referring to?
 

yerrag

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What are you referring to?
I think this forum needs to understand this well.
Another interesting pattern I see in covid19 recovery group is the claim it’s like chronic fatigue syndrome, the thing is many of them claim they were perfectly healthy, if you look into it you find it’s full of long distance runners, tri-fit types, triathlons and the like. This lot basically run on cortisol after years of doing that, many are over 30 and doing excessive exercise for years and don’t have the same recovery as they had in their 20’s with regard to protective hormones.
I was answering to this..People being dependent on cortisol, and cortisol happens with poor blood sugar regulation.

If there is good sugar regulation, and there's never a sugar low, there's no need for cortisol to be produced.
 

lvysaur

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I was answering to this..People being dependent on cortisol, and cortisol happens with poor blood sugar regulation.
Yes, but what do you mean by the "Many like to talk SFA but don't walk the talk. No one goes on a 4yr PUFA cold turkey intervention."
 

yerrag

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Many like to talk SFA but don't walk the talk. No one goes on a 4yr PUFA cold turkey intervention."

Means people here believe SFAs are good, and PUFAs are bad. Too much PUFA fatty acids in the blood blocks glucose metabolism.

If they believe that to be the case, they should not only keep from eating foods having PUFAs. Not only that, they should even commit to 4 years of restriction from PUFAs continually, so that over that period, the PUFA fatty acids coming from their fat stores will slowly be metabolized and be gone from the system. Ray Peat has talked about that, and to date I have only seen one member, apart from me, say to have done that. In my 4 years as a member in RPF.
 

rei

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covid is an innate exosome response, not a infectious disease. When the immune system first notices that there is undesired signalling it starts to mount "attacks" or better described as homeostasis restoring strategies. Antibodies to mop up the exosomes and if needed T cells that directly shut down cells that are stuck in a stressed state and producing the exosomes.

PUFA restriction is only relevant in the sense that it allows your immune system to keep working at a more effective level as it does not need to tend to PUFA damaged cells. A PUFA damaged cell is also the one that had covid inserted using linolenic acid.

But please do understand, this corona cannot cause symptoms in you if you have even a halfway-normally working immune system. Air pollution combined with lack of vitamin d and especially sunlight is the best predictor of expression of coronavirus exosomes, and severity of disease.

Using a mask will make "catching the disease" more probable, as it filters out all large droplets that would get analyzed and acted upon at the tonsils or other peripheral immune hubs. When only microparticles get through and go into the lungs mainly, the immune system first needs to detect them there, then travel to immune hubs, and then start the response after immune hub is taught the signature. During this time the lungs are completely exposed and executing the wrong adpatation program, making it possible a fever or worse develops instead of staying asymptomatic.

exactly like decades of people dumb enough to fall for the vegetable oil scam were culled from the population, now the virus hysterics are. Using the same method, voluntarily harming themselves to death due to their religious belief. Vaccinations have done the same continuously for a much longer time.

My only real fear for the future is that the eugenicists get so bold the mandate things instead of relying on people voluntarily doing it.
 
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yerrag

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PUFA restriction is only relevant in the sense that it allows your immune system to keep working at a more effective level as it does not need to tend to PUFA damaged cells.
No PUFA means better blood sugar regulation, making one closer to attaining optimal blood sugar regulation. When optimal, stress hormones are minimized. Low cortisol, low insulin, low PTH. Low cortisol - better thymus gland functionality - more T-cell that can mature. Low insulin- more endogenous production of vitamin D. With activated vitamin D, and with dietary calcium intake, low PTH results.

Low PUFAs is very important. The cascade effect stemming from high PUFAs in the system stemming for its effect on blood sugar regulation is systemic.

I did not mention the effect on energy production, which is more evident in this forum.
 
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