Merrill Chase Inadvertently Disproved Antibodies in 1942
Inadvertently: without knowledge or intent
When I first began uncovering the fraud of virology, I was still somehow convinced that there was such a thing as an “immune system” that utilized substances called “antibodies” in order to protect us from outside pathogens. While I understood that vaccination was dangerous due to the toxic recipes used in their creation, my counter to those pushing for vaccine-acquired “immunity” was to argue in support of naturally acquired “herd-immunity.” I was stuck in this false-binary paradigm as I was still working through the unscientific methodologies used by virologists to claim that invisible pathogenic “viruses” existed. I also had not let go of the idea that bacteria and fungi were invading pathogens as I had not expanded the scope of my inquiries to go beyond “viruses” at that time, and I had yet to truly understand the terrain theory.
It wasn't until I fully understood the importance of purification and isolation procedures for establishing a valid independent variable when using biological materials, as well as the lack of adherence to the scientific method in the virology literature, that I began to question “antibodies” and the entire concept of “immunity” as they are so closely intertwined. For anyone unfamiliar, purification means that a substance is free of any contaminants, pollutants, foreign materials, etc. that debase it, whereas isolation refers to the complete separation of one thing from everything else. In regard to virology, this should mean that the “viral” particles are separated entirely in a single form away from any host and foreign materials, cell debris, contaminants, etc. However, the meanings for both purification and isolation have been debased in virology and do not represent the common understanding of the words. One of the common excuses used by researchers for the inability to completely purify and isolate “viruses” prior to any experiments taking place is that they are too small, and therefore, the “viral” particles will collect and co-sediment with any similar particles that are of the same size and density. It is admitted by researchers that the technology needed to completely separate the assumed “viral” particles even from extracellular vesicles such as “exosomes” that are of the same size and density, does not exist. Thus, complete purification and isolation is unable to be achieved in order to have a valid independent variable for study.
Since typical “viruses” range from 20 to 300 nanometers (nm) in diameter and “antibodies” are said to be much smaller, around 10 nm, it became clear to me that if researchers cannot purify and isolate “viruses” directly from a sick host in order to manipulate them in experiments, they would also be unable to do this for the even smaller “antibody” particles. This line of inquiry led me to examine the pivotal moments in the history of “antibody” research, beginning with papers written in 1890, in order to uncover how these entities were discovered and how they had their functioning determined. Upon doing so, I came to the realization that the same problems affecting “viruses” applied to “antibodies,” specifically in regard to the inability to purify and isolate the assumed “antibodies” in order to have them on hand to vary and manipulate during experimentation. Like “viruses,” the “antibody” was a hypothetical entity that was created to explain unnatural reactions observed when mixing blood from different species with various chemicals in Petri dishes. These particles were purely (pun somewhat intended) an imaginary concept, and were unable to be directly observed. I found out that there were no less than six different theories proposed over the course of decades trying to describe how these invisible particles form and function due to the inability to actually witness the processes that they were claimed to be involved in. On top of these problems, I also became aware of the issues with the lack of specificity of the hypothetical “antibodies” to react and bind only to their intended target. This caused many problems for the research papers written using these entities, resulting in a reproducibility crisis where researchers have been unable to reproduce and replicate their own findings as well as those of their peers due to the inconsistent reactions observed within the lab.
It was a long rabbit hole to go through, and there are still a few articles in need of being updated for the ViroLIEgy.com site. When it is all completed, I plan to do a summarized write-up of the timeline and findings in the future. However, until then, here are the articles in a mostly chronological order based upon the date of the “discoveries.”
Emil Von Behring’s Diphtheria/Tetanus Papers (1890): Precursor to Antibodies
Paul Ehrlich’s Side-Chain Antibody Theory (1900) Part 2: The Complement System
Direct Template and the Theoretical Structure of Antibodies (1930-1940)
Was the First Atomic Resolution Structure of an Antibody Fragment Published in 1973?
In order to complete this investigation into “antibodies,” I have updated one of the last articles that I had written as a part of this effort, originally posted to Facebook back on May 4th, 2021. The research covered in this article took place in 1942 and 1947. Thus, it is a little out of order in the chronological timeline. However, the findings were not deemed significant until later, and I had initially stumbled upon it at the end of my investigation. The work presented below is from immunologist Merrill Chase, and it demonstrates how the researcher inadvertently disproved the notion that “antibodies” result in “immunity,” a guiding principle behind the vaccination scam.
In 1942, Rockefeller immunologist Merrill Chase, along with his Rockefeller co-hort biologist, physician, and immunologist Karl Landsteiner, accidentally disproved the notion that “antibodies” protected the body against “infectious” disease. This came about due to the researchers desire to understand how “immunity” against tuberculosis could be transferred. The researchers attempted to gain a better understanding by studying a process known as sensitization, which is where an organism is exposed to an antigen (any toxins or substance believed to trigger “immune” reactions) in order to induce an “immune” response, thereby theoretically preparing the “immune” system to react more strongly and rapidly upon subsequent exposures to the same antigen. According to Rockefeller author (seeing a connection?) Carol L. Moberg in her 2015 paper on Merrill Chase, it was Landsteiner’s belief that, if “sensitization” with a simple chemical produced an “immune” reaction, a cell-bound “antibody” would reside in the tissues of the “sensitized” animal. He believed that this “sensitization” could be transferred by injections of clarified serum from peritoneal exudates to a normal animal.
To try and unlock this mechanism, it was Chase who attempted to “sensitize” guinea pigs by exposing them to an antigen (tuberculin in this instance) in order to produce this specific hypersensitivity “immune” response. Once they observed a hypersensitivity “immune” response, Chase took the blood serum from an “immunized” guinea pig that was said to contain only the so-called “antibodies,” and then injected this into healthy “non-immunized” guinea pigs. When challenged with the antigen, the researchers looked once again for a localized inflammatory response at the site of the tuberculin injection, which is supposed to be indicative of the “immune” system's heightened sensitivity to the antigen. However, to his surprise, upon challenging the guinea pigs, Chase was unable to transfer "immunity" utilizing the serum containing only the “antibodies.” During his experiments, he was only able to obtain the reaction and grant “immunity” when he used white blood cells. Merrill Chase described this moment in his 1985 paper Immunology and Experimental Determitology:
“In the course of these futile exercises, I once transferred the sticky exudate when it was not fully clarified, but had a hint of opacity. The recipient of this became beautifully positive. The following experiment, with fulIy clarified fluid, was negative-and then I knew. When Landsteiner looked through the microscope and saw lymphocytes, he did an abrupt about-face and said, with dignity, "Yes, I thought so!" Had he suddenly recalled the work of James B. Murphy on lymphocytes, begun in 1912 and summarized in a monograph in 1926 (16)?”
Chase recounted this moment as well in a 1988 paper that he wrote titled Early Days in Cellular Immunology:
“Such exudates were transferred to naive guinea pigs, but the recipients did not react to TNCB applied topically in triglyceride oil. Once during the course of these trials, I did not fully clarify the exudate-and frank contact sensitivity arose in the recipient. The exudate cells were almost exclusively Iymphocytes.”
Notice that Chase stated that he clarified the sample. This is not the same as purifying a sample. Clarification is an initial step aimed at removing large particles, cell debris, and other insoluble impurities from a biological sample. The resulting solution would still theoretically contain substances beyond the supposed “antibodies” such as soluble proteins, nucleic acids, and other small impurities. Purification, on the other hand, is meant to isolate the “antibodies” from the clarified solution to obtain a highly concentrated and pure sample. The goal is to remove as many contaminants as possible, including proteins, nucleic acids, lipids, and other substances, in order for the sample containing only the “antibodies” to be utilized for structural, functional, and biochemical studies. Thus, we can see that it is an assumption on the part of Chase that his clarified sample had any of the hypothetical “antibodies” present.
Nonetheless, Chase went on to point out that Astrid Fagraeus, who had come up with the idea that “antibodies” are derived from plasma cells in 1948, had noted that they were not present in his samples. This meant that, according to the accepted fictional narrative about how the hypothetical “antibodies” supposedly form, the sensitizing protocol Chase used was effective for inducing contact sensitivity, a type of cell-mediated “immune” response that is separate from an “antibody-mediated” response, as there were no “antibodies” present.
“Astrid Fagraeus, who in 1948 had pointed out the relation between antibody-production and plasma cells (blast forms) in rabbit tissues, came to my laboratory and studied stained smears of the transfer cells. After long search, she looked up and remarked, "No, there are no plasma cells in your exudate." So, according to the sensitizing protocol being used, we could effect only contact sensitivity; or both contact sensitivity and antibody-synthesis by cells-indistinguishable under the microscope.”
Chase stated that, even in the extraction of large volumes of splenic and nodal cells, regardless of their belief that “antibodies” were being “synthesized” inside the animal, no “antibodies” could be detected at all.
“With the cells that gave rise to circulating antibody in our experiments, the on-going synthesis was so low at the time of transfer that none could be detected by passive cutaneous anaphylaxis upon extraction of large volumes of splenic or nodal cells.”
Instead of realizing from these experiments that what they had done had falsified the hypothesis that the assumed-to-be-present “antibodies” offered “immunity,” Chase decided to extend to the field of immunology a rescue device in order to save face. The researcher conjured up the idea that there was not only the one “antibody” system protecting us from disease, but that there were actually two different components of the “immune” system that acted at different times. These two systems became known as the immediate INNATE response (cell mediated) and the delayed ADAPTIVE response (“antibody” mediated).
We can confirm these accounts by examining two of the papers that Chase wrote during the 1940s. The first, presented in its entirety, is Merrill Chase's 1942 paper with Karl Landsteiner. It is a brief notice that confirms that the reactions from the guinea pigs were caused by the sediment obtained after centrifugation and not by the clarified fluid said to contain “antibodies.” Chase felt that an active sensitization through residual antigenic material was improbable and that he was inclined to assume that the sensitivity was produced by the activity of the remaining cells in the unclarified fluid. Chase concluded that attributing reactions to anaphylactic antibodies needed further investigation (obviously these investigations didn't pan out).
Experiments on Transfer of Cutaneous Sensitivity to Simple Compounds.
In the course of experiments to passively transfer skin sensitiveness to simple compounds an attempt was made to induce sensitivity by injecting peritoneal exudates from sensitized animals. Guinea pigs were rendered sensitive to picryl chloride in the manner previously described, using conjugates (guinea pig stromata treated with picryl chloride) in conjunction with intraperitoneal injections of killed tubercule bacilli. To produce exudates, killed tubercle bacilli (or tuberculin) were injected intraperitoneally about 3 weeks from the beginning of the treatment, when substantial tuberculin hypersensitivity was established.
On injecting such exudates intraperitoneally into normal animals, the recipients in most of the experirnents were seen to develop sensitivity to picryl chloride; when then a drop of an oil solution of the substance was put on the skin, erythemiatous reactions, mostly of high color, were apparent on the next day. The phenomenon was found to be due not to the clarified fluid but to the sediment obtained upon centrifugation. Among the possible exexplanations an active sensitization through residual antigenic material in the peritoneal exudates seems rather improbable because a transfer was possible also with the exudate of animals in which the injection of dead tubercle bacilli and picryl stromata was made under the skin of the neck (using as a vehicle “Aquaphor” (Duke Laboratories) and paraffin oil, according to a method devised by Freund). This is further supported by the appearance of the sensitivity after a short interval, namely, 2 days after injection of sufficient material, and fading of the reactivity within a few days. Finally, there is preliminary evidence that moderate heating sufficient to kill the exudate cells abolishes the effect. Consequently one would be inclined to assume that the sensitivity is produced by an activity in the recipient of the surviving cells, if not by antibodies carried hy these. Positive results were obtained with about 1.5 cc of sediment, which were given in 3 portions on successive days or all at one time; with the present procedure this necessitates the use of quite a number of donors.
Definite results have been obtained with an acylchloride, o-chloro-benzoyl chloride: the majority of experiments have been made with citraconic anhydride, one of the acid anhydrides shown by Jacobs, et al. to produce a new and particular form of reaction (in animals), namely, urticaria-like reactions often with pseudopods appearing immediately after a scratch-test. Positive transfer in human beings had been mentioned briefly by Kern with serum from a patient sensitive to phthalic anhydride, suggesting further experimental study (vide Jacobs). We found that sera from highly sensitive guinea pigs which have received intensive treatment with intracutaneous injections of oil solutions of citraconic anhydride contain an antibody which upon intraperitoneal injection into normal guinea pigs render them sensitive. Upon scratch tests made through a drop of a solution of this incitant in dioxane, the recipients gave reactions similar to the immediate ones seen in actively but not highly sensitized guinea pigs. However, upon intracutaneous injection of potent sera (amounts of 0.15 to 0.05 cc were used) into normal albino guinea pigs, intense reactions were elicited within a few minutes in scratch tests made on the prepared site, consisting in swelling arid a pinkish coloration, most often with pseudopods and extending over an area up to 3 cm in diameter. The color receded within an hour or so, whereas the swelling persisted for several hours more; the next day the reaction was no longer present. Such reactions occurred in the sensitized sites also when the scratch test was made elsewhere on the normal skin or an oil solution was injected subcutaneously. Furthermore, reactions, even stronger ones (c. g., 5 cm x 4 cm), were obtained at the prepared sites upon subcutaneous injections of the conjugate made with citraconic anhydride and guinea pig serum. The prepared areas were commonly tested after one or two days but are still well reactive after 3 days. Whether the immediate skin reaction described is attributable to an anaphylactic antibody is being investigated. The essential facts are recapitulated in Table I.
https://journals.sagepub.com/doi/abs/10.3181/00379727-49-13670
https://doi.org/10.3181%2F00379727-49-13670
According to Moberg, Chase stated that Landsteiner was reluctant to report the details of their findings beyond the above brief notice from 1942 as he was skeptical that others could reproduce their results. However, Chase knew of seven researchers who had immediately confirmed their findings. Regardless, after Landsteiner’s death in 1943, Chase did not follow-up on their work until 1947.
“In retrospect, it may seem curious why full details of this significant discovery were never reported and thus not widely known for a long time, though the work did appear as a brief notice in Proceedings of the Society for Experimental Biology and Medicine in 1942. Chase said Landsteiner was skeptical that anyone could reproduce their results. Even though Chase knew that seven other scientists almost immediately confirmed those results, his own insecurity on Landsteiner’s death in 1943 and his uncertain future at Rockefeller kept him from writing up the experiments—something he much later regretted.
When Dubos reported to Rockefeller Scientific Director Herbert Gasser that Chase’s linking of the lymphocyte to the formation of hypersensitivity opened “an entirely new immunological vista,” Gasser appointed Chase to the Dubos laboratory, which was just beginning a study of tuberculosis. In an extension of his experiments with Landsteiner, Chase transferred hypersensitivity to tuberculin (a purified protein derived from mycobacteria) from a sensitized guinea pig to a nonsensitized one by injecting sensitized white blood cells. Chase and Dubos then realized that certain white cells were not mere carriers of antibody but served in its production; and, importantly, that hypersensitivity to tuberculin was not equivalent to having tuberculosis. In other words, a positive tuberculin test does not necessarily measure active disease, only allergy or previous sensitization to the protein. This reaction, shown by Chase in guinea pigs, was soon secured in humans by H. S. Lawrence and W. S. Tillett at New York University."
In 1947, Chase wrote the paper detailing his experiments investigating the mechanisms behind cutaneous hypersensitivity reactions in response to tuberculin, which is used in tuberculosis testing. In his experiments, Chase demonstrated that the guinea pigs that received lymphocytes from the sensitized donors developed cutaneous hypersensitivity to tuberculin, whereas when he utilized the serum containing “antibodies,” he was unable to produce the same hypersensitivity response in the recipient guinea pigs. It was this work that was considered foundational for establishing that certain “immune responses,” such as hypersensitivity reactions, use cells rather than “antibodies.” I am providing the two most relevant passages from the paper that highlight these findings, while the rest of the paper can be found at the link.
The Cellular Transfer of Cutaneous Hypersensitivity to Tuberculin.
“In studies on experimental drug allergy, it to has been found that specific hypersensitiveness of the “delayed type” is transferable to normal guinea pigs by means of cells in exudates recovered from sensitized guinea pigs. Resemblances between the delayed type of reaction to drugs and the classical tuberculin reaction have prompted investigation as to whether cells from tuberculin-sensitive animals may likewise transfer tuberculin sensitivity. The experiments show that guinea pigs receiving such cells acquire for a limited time a skin hypersensitivity that exhibits the essential features of the typical tuberculin reaction.”
“In contrast to the reactions following upon the injection of washed cells, similar effects have not been obtainable with serum of the donors of active cells, or with cells from normal animals.”
https://journals.sagepub.com/doi/abs/10.3181/00379727-59-15006P
https://doi.org/10.3181/00379727-59-15006P
The New York Times summarized the “importance” of Chase's findings upon his death in 2004, noting that his research undermined the longstanding belief that “antibodies” alone protected the body from microorganisms and disease. The widespread tenet at the time was that “antibodies” circulating in the bloodstream attacked invading “pathogens” in order to protect the body. However, Chase's results shattered this tenet and his findings were used to redefine the “immune” system concept, even though it generated little interest at the time:
Merrill W. Chase, 98, Scientist Who Advanced Immunology
“Dr. Merrill W. Chase, an immunologist whose research on white blood cells helped undermine the longstanding belief that antibodies alone protected the body from disease and micro-organisms, died on Jan. 5 at his home in New York City, according to the Rockefeller University, where he worked for 70 years. He was 98.
Dr. Chase made his landmark discovery in the early 1940's while working with Dr. Karl Landsteiner, a Nobel laureate recognized for his work identifying the human blood groups. At the time, experts believed that the body mounted its attacks against pathogens primarily through antibodies circulating in the blood stream, known as humoral immunity.
But Dr. Chase, working in his laboratory, stumbled upon something that appeared to shatter that widespread tenet.
As he tried to immunize a guinea pig against a disease using antibodies he had extracted from a second pig, he found that blood serum did not work as the transfer agent.
Not until he used white blood cells did the immunity carry over to the other guinea pig, providing solid evidence that it could not be antibodies alone orchestrating the body's immune response.
Dr. Chase had uncovered the second arm of the immune system, or cell-mediated immunity. His finding became the groundwork for later research that pinpointed B cells, T cells and other types of white blood cells as the body's central safeguards against infection.
''This was a major discovery because everyone now thinks of the immune response in two parts, and in many instances it's the cellular components that are more important,'' said Dr. Michel Nussenzweig, a professor of immunology at Rockefeller. ''Before Chase, there was only humoral immunity. After him, there was humoral and cellular immunity.''
Dr. Chase's breakthrough generated little interest at the time, but it set in motion the research that helped redefine the fundamental nature of the immune system.”
The British Society of Immunology provided a similar account of Chase's work, noting that he failed to transfer “immunity” when using serum supposedly containing “antibodies,” and that he inadvertently used supernatant containing white blood cells in order to get the sensitivity reaction that he wanted. In other words, the discovery of the “innate immune system,” which does not rely upon hypothetical “antibodies” at all, was a happy accident.
Guinea pig (1942)
“One of the most important immunology experiments carried out with the help of guinea pigs was published in 1942 by Karl Landsteiner and Merrill Chase of the Rockefeller Institute for Medical Research in New York. They were investigating the transfer of sensitivity to specific antigens from an immunised guinea pig to another “naïve” animal.
At that time, it was known that it was possible to transfer antibodies from one animal to another to make them sensitive to an antigen. However, when Chase tried to transfer the sensitivity by injecting serum from immunised guinea pigs into non-immunised, naïve animals, he failed. But when he inadvertently used a supernatant fluid that had not been prepared as well as other preparations, the naïve guinea pigs developed the typical skin reactivity indicating that the sensitisation had indeed been successfully transferred.
Perplexed by the result, Chase looked under the microscope and found that the cell-free supernatant was not cell free at all but contained lymphocytes. In effect, he had discovered what is now called cell-mediated immunity, which worked in quite a different way to antibody-mediated immunity. Cell-mediated immunity does not involve antibodies, but rather the activation of cytotoxic T-lymphocytes in response to contact with an antigen. Chase went on to repeat the experiment with M. tuberculosis and concluded that both sets of reactions where due to the presence of lymphocytes. These experiments established the dichotomy of immediate (antibody mediated) and delayed (cell mediated) immune responses.”
https://www.immunology.org/guinea-pig-1942
One final commentary on Chase's work reiterated that he showed that he could sensitize animals in the absence of detectable “antibody” production. However, at the time, it was controversial whether he had truly demonstrated an “antibody-independent” response, most likely as they feared the consequences of Chase's contradictory evidence.
Dual Arms of Adaptive Immunity: Division of Labor and Collaboration between B and T Cells
At the time, it was thought that antibodies, or other chemical substances in the bloodstream, were the principal mediators of immunity. However, Chase showed that passive transfer of white blood cells could sensitize an animal to the original sensitizing chemical even in the absence of detectable antibody production in a process called contact allergy or delayed-type hypersensitivity. This was a landmark discovery of a new class of immune response termed “cell-mediated immunity”; however, it remained controversial whether or not this was truly an antibody-independent process (Chase, 1985). Chase’s observations did not postulate a division of labor between cellular and humoral immunity and left unresolved the question of where antibodies came from, the relation between antibodies and white blood cells, and how animals specifically developed and adapted their immune responses to different kinds of pathogens.”
https://www.sciencedirect.com/science/article/pii/S0092867419309109
To summarize, Merrill Chase injected guinea pigs with an antigen (tuberculin) to induce a hypersensitivity reaction, which was an effect that was used as a marker of “immunity.” He then took blood from these “immunized” guinea pigs and clarified it to a point where he believed only “antibodies” remained. Injecting this clarified blood into “non-immunized” guinea pigs did not result in a hypersensitivity reaction. However, when he used less clarified samples that still contained blood cells, the “non-immunized” guinea pigs did exhibit a hypersensitivity reaction. This led Chase to conclude that it was not the “antibodies,” but the blood cells, that were responsible for transferring “immunity,” as evidenced by the observed hypersensitivity reaction. As is the case in virology, Chase used lab-created effects in order to determine the role of an invisible entity, and then accidentally disproved the role that this entity was associated with during his experiments.
Merrill Chase admitted that they could not detect plasma cells or “antibodies” in their experiments (only lymphocytes), and then assumed that “antibodies” formed inside the body of the animal by other unseen and delayed means. However, as the researchers could not pass “immunity” through the use of serum containing supposed “antibodies,” only with the serum containing white blood cells, Merrill Chase had falsified the unscientific hypothesis that “antibodies” are responsible for “immunity.” Yet, instead of admitting that they were wrong about the existence of the unseen “antibodies” and their assigned theoretical function when the researchers were unable to produce an “immune” response using serum said to contain these invisible entities, it was decided to split the “immune” system into two different responses, and the B cells were given the ability by Astrid Fagraeus to create these hypothetical substances. By establishing the dual concepts of innate and adaptive “immunity,” immunology could keep their unproven “antibody” theory in the face of contradictory evidence. Despite the fact that the hypothesis had been falsified, the fiction was reworked in order for immunology to sweep away any results where “antibodies” are not detected or do not grant “immunity” when they are supposed to do so. This pivotal moment in establishing a pseudoscientific rescue device allowed the concept of vaccine-acquired “immunity” to move forward, needlessly endangering and harming many future generations in the process.
The Baileys examined anthrax and the bio weapon narrative.
The Baileys also announced another member joining the “No Virus” position in Pierre Chaillot, a statistician and author from France.
had a plethora of Freedom of Information requests:H5N1:
Failed “Virus” and Fluoride Challenges:
Hepatitis C:
Group A Streptococcus:
looked at why we do not need to be afraid of mosquitoes. provided an investigation into the “SARS-COV-2” sequencing sham. explored whether parasites are friend or foe. explained how smallpox is measles, measles is chickenpox and chickenpox is smallpox.
It’s almost to the level of irony that the concept of an “immune system,” invented to explain why many are not affected by supposed pathogens, has another fantasy layer added by inventing an explanation for why “antibodies” also don’t work as theorized. It does become easy to see, if it wasn’t before, how money and professional reputation are much more important in “scientific research” than finding out how biology actually works—and being willing to have one’s ideas be proven wrong. Thanks for another revealing essay, Mike!
If you thought the vax market is big, you should see the antibody market. Another lucrative industry that has spawned from the unproven virus hypothesis. $equence$ $ATCG$
Vaccines:
https://www.marketsandmarkets.com/Market-Reports/vaccine-technologies-market-1155.html
Antibodies:
https://www.marketsandmarkets.com/Market-Reports/antibody-therapeutics-market-178852478.html