Antibodies AFTER vaccines do NOT mean immunity

Antibodies are just one aspect of the immune system. They show there has been exposure. PERIOD. If there are antibodies after experiencing a disease, they may mean immunity as the rest of the immune system was mobilized - all aspects. With vaccines, much of the immune system is bypassed - TH1 (mouth, nose, throat and all aspects of immune system that gets mobilized there). Only TH2 responds (simplified a bit here). So antibodies do NOT mean immunity. All aspects need to be measured and for the most part they have no clue how to do that or even what to measure and what actually indicates immunity.

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 oher 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.

"So many areas of medicine rely on this type of reaction that he clearly distinguished as not being antibody mediated," said Dr. Ralph Steinman, a professor of cellular physiology and immunology at Rockefeller. "People never anticipated that there would be something other than antibodies. It was an amazing finding."

Born in Providence, R.I., in 1905, Merrill Wallace Chase earned his bachelor's degree and doctorate from Brown. He taught biology there for a year, before joining the faculty at Rockefeller in 1932 as an assistant to Dr. Landsteiner. He has published at least 150 scientific papers.

In 1975, he was elected to the National Academy of Sciences

Hi Jamie,

>But Meryl, why are you aking me a question when you already know what my answer will be. I have no doubt you could explain my point of view much better than I. :)

Well, two reasons, I guess. One is to play the devil's advocate a bit ;-) I mean, I was brought up in a house where we were not happy unless we were having a discussion about two sides of some issue. Debating was a family hobby. Also, I was interested to hear what your reasoning was and to be honest, I have to say that you have learned what they taught you in school - very well, I'm sure. But you have not done any investigation on your own.

For instance, the theory that antibodies = protection from disease was disproven a long time ago. And I mean a LONG TIME! Study after study has shown that people with high levels of serum antibodies have contracted illnesses they are serologically immune to whilst those with low to no antibodies have been protected. I will quote below a section from an article on Polio vaccine which is coming out in the next issue of Informed Choice Magazine:

"Two studies which were published in 1939 and 1942, investigated the diphtheria antibody concentration in people who contracted diphtheria in England and Wales. It reported, "on repeated occasions, it was found that a sample of serum, taken from a patient with a clear history of inoculation who had yielded diphtheria bacilli from nose or throat swabs (a sure sign of diphtheria infection) .was found to contain quite large quantities of diphtheria antitoxin." (in other words, they were serologically immune to diphtheria yet they contracted it) Ironically, they found, ".the occurrence of several instances of non-inoculated persons having no circulating antitoxin, harbouring virulent organisms and yet remaining perfectly well." (they were unvaccinated, had active diphtheria bacteria detectable in their nose and throat and yet displayed no symptoms of illness).

We know now and have known for over 60 years that our method of measuring immunity is completely wrong. Despite this, we continue to use these useless tests to show that vaccinates work because after vaccination someone develops antibodies!"

You said that: "To answer your question more directly: natural infection will stimulate antibodies, but often too late. And, natural infection (when you survive) doesn't protect you against future infection."

And yet, think about it Jamie. If the antibody production from natural infection will not protect you from future infection (which you admit it will not), then how will the antibodies from vaccines do so? Also, since tetanus and diphtheria are both toxin-mediated illnesses (as is pertussis), how can antibodies EVER prevent the multiplication of toxin since, upon exposure to our own body's natural defenses, clostridium tetanii, bordetella pertussis and diphtheria will ALL produce toxins which, regardless of our antibody status, will produce symptoms of infection?

So, to boil it down to two questions:

1- if as has been shown in studies, the existence of antibodies does not equal immunity to infection, how can we show that vaccines protect?

2- If the production of antibodies does not protect against toxin-mediated diseases, why do we continue to vaccinate against them?

Take care, Meryl

Bronwyn's Website - Vaccination Information Service (this is not on the website)

I would say Meryl that you are not immune in the technical sense, but at the same time you are not susceptible, if that makes sense to you. At least you weren't susceptible when you were exposed to it anyway. A mother had her daughter sleep at the home of another couple of children who had chicken pox so that she could contract it, and she did not for ages, though she eventually did after 6 weeks. It is apparent that the body will only contract a particular disease if and when it needs to, and it may be that you could go all your life without it ever needing to, even though you are not fully immune. I think it is good to have the exposure though, because then at least the body has the opportunity to go through it if it will benefit from it.

Many factors would influence our susceptibility to contracting a particular infection in the first place, including health (which is affected by nutrition, clean water, fresh air, etc), mental state, genes and the body's metabolism and biorhythms.

So, if immunity can't be measured by the level of serum antibodies, does anyone know of any other tests that can be performed to determine immunity?

If antibodies ARE present, and the person has not been vaccinated, then you would know that the antibodies were produced as a result of going through the disease naturally, which does bring immunity, provided the immune system is functioning normally.

So combining all of the above, .... antibodies in non-vaccinated person will signal immunity. If you do NOT have antibodies though, you still do not know if you are susceptible or not.

By the way, (vaccine) research has found that IgA antibodies are a much better indication of immunity than IgG antibodies, but when you have gone through the infection naturally (i.e. the antigen has entered through the natural portals of entry), both would be present anyway. When you inject the vaccine ingredients directly into the system, however, you basically bypass the production of IgA, which is another reason why we know immunologically that vaccines are ineffective. Indeed it is the quiet realisation of this significant error that is prompting efforts to produce vaccines that are inhaled instead of injected, e.g. the 'flu vaccine (though they will still be pointless and contain harmful ingredients).

It has been theorised by some that vaccines overstimulate the humoral immune response (which incorporates the production of antibodies) at the expense of the other major part of the immune system - the cell-mediated immune response (the production of T cells). I would say that even this is being too kind to vaccines, because it clearly does not even stimulate a normal humoral immune response. The immune system is very complex and with important inter-relationships between its components. The development of immunity requires many processes to occur and complete, requiring the whole team work of all the required immune system components. This simply will not occur other than when the body contracts the infection naturally, and this is only when IT, THE BODY, wants to, not when man wants it to, say at 3:15 in the afternoon between getting the shopping done and going around to leave baby at nanna's in time to get to the gym, etc.

Bronwyn

What are the limits of adjuvanticity? Del Giudice G, Podda A, Rappuoli R.
IRIS Research Center, Chiron SpA, Via Fiorentina 1, 53100, Siena, Italy.
Vaccines developed traditionally following empirical approaches have often limited problems of immunogenicity, probably due to the low level of purity of the active component(s) they contain. The application of new technologies to vaccine development is leading to the production of purer (e.g. recombinant) antigens which, however, tend to have a poorer immunogenicity as compared to vaccines of the previous generation. The search for new vaccine adjuvants involves issues related to their potential limits. Since the introduction of aluminium salts as vaccine adjuvants more than 70 years ago, only one adjuvant has been licensed for human use. The development of some of these new vaccine adjuvants has been hampered by their inacceptable reactogenicity. In addition, some adjuvants work strongly with some antigens but not with others, thus, limiting their potentially widespread use. The need to deliver vaccines via alternative routes of administration (e.g. the mucosal routes) in order to enhance their efficacy and compliance has set new requirements in basic and applied research to evaluate their efficacy and safety. Cholera toxin (CT) and labile enterotoxin (LT) mutants given along with intranasal or oral vaccines are strong candidates as mucosal adjuvants. Their potential reactogenicity is still matter of discussions, although available data support the notion that the effects due to their binding to the cells and those due to the enzymatic activity can be kept separated. Finally, adjuvanticity is more often evaluated in terms of antigen-specific antibody titers induced after parenteral immunization. It is known that, in many instances, antigen-specific antibody titers do not correlate with protection. In addition, very little is known on parameters of cell-mediated immunity which could be considered as surrogates of protection. Tailoring of new adjuvants for the development of vaccines with improved immunogenicity/efficacy and reduced reactogenicity will represent one of the major challenges of the ongoing vaccine-oriented research.

PMID: 11587808 [PubMed - indexed for MEDLINE]

Many great quotes demonstrating that antibodies after vaccines do NOT mean immunity