Tovaxin, oh and abx...

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Tovaxin, oh and abx...

Postby CureOrBust » Sun Nov 13, 2005 3:30 am

Just a thought which keeps bugging me.

Tovaxin (the MS "vaccine") appears really positive. And from my understanding, its based around killing the immune cells that attack myelin. The doctors breed these from the sufferers own blood.

The thought is, it would be interesting to see if these same T-cells would attack, oh, i dont know, say CPn.
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Postby gibbledygook » Sun Nov 13, 2005 7:52 am

I am totally in agreement with your doubts! How can an immune suppressant help if the disease is caused by an infection? Might Tovaxin be merely treating the symptoms rather than the cause? Might the antibiotics be a diversion? Unfortunately I don't think the answers are available yet. And antibiotics are cheap and relatively safe and available so I'm going to stick with them until they release Tovaxin. If they release it.
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Postby EricJohnson » Mon Nov 14, 2005 10:44 am

Tovaxin sounds scientifically interesting. Does it cause particular subsets of T-cells to be depleted, or all T-cells?

I am totally in agreement with your doubts! How can an immune suppressant help if the disease is caused by an infection?


A good inquiry to make. One possibility is that because the immune response is always present in a pathogens environment, the pathogen could evolve dependancies on it. For example, a pathogen could evolve to target white cells. When the amount of white cell infiltrate goes down due to say prednisone, the pathogen cannot reproduce as quickly.

This idea is rather speculative, and anyway the Prineas and Barnett finding strongly questions the notion that white cells present in the brain are the keystone of MS.

More usefully perhaps, you may be able to find some examples in the literature, where diseases or cases accepted to be infectious do respond to steroids without generally causing a total disaster is the long run. Such a thing sounds vaguely familiar but I cant say for sure whether I have seen it.
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Postby CureOrBust » Tue Nov 15, 2005 12:06 am

EricJohnson wrote:Tovaxin sounds scientifically interesting. Does it cause particular subsets of T-cells to be depleted, or all T-cells?


From what I have read (and seen on their movie) they get your blood, identify which of YOUR t-cells have an appetitie for myelin, culture these in bulk, radiate these so they are non replicating, and so that when they are re-introduced into your body, you develop an imune reaction that kills these specific t-cells. ie only the myelin hungry t-cells are targetted, not every t-cell. very interesting.


gibbledygook wrote:I am totally in agreement with your doubts! How can an immune suppressant help if the disease is caused by an infection?

I think you mis-read me, I am actually very interested in this technology. I am just interested if this same t-cell attacks some particular bacteria also by chance.

Two things I note are that the treatment is given monthly, which implies it is reversible to me. And secondly, our use of abx from my understanding is to not to boost our immune system, but to do what it cant do. so I personnally am not too concerned about loosing a couple (million...) myelin eating t-cells. I take abx to kill any possible infection.
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Postby EricJohnson » Sat Nov 19, 2005 12:50 pm

I'm reading the Hellings and van der Aa paper on this treatment. They say there is indeed an anti-idiotypic response, that means the response against the particular (antimyelin) T-cell clones.

But they also say there is an anti-ergotypic response, which is a response against molecules which all T-cells up-regulate when they are active. This response would be expected to depress T-cell-mediated immunity generally.

The authors dont seem(?) to have come to a conclusion regarding whether the specific or nonspecific immunological effects were more responsible for the clinical effects.

There are other papers out there on this topic - one can put [ms autologous t-cell vaccination] in pubmed. Some of them may use different treatment protocols, etc, or just have different opinions or get different results. Also this study was very small. So the findings of this paper dont necessarily tell you everything you might want to know. I am kinda tired & bummed to read anymore right now tho. Also, one should work thru this paper persoanlly if it really matters to one, as I have read it a little lazily.

Random question, does anyone know if anti-Cpn T-cells (not antibody) have been looked for in MS brain/CSF? That would be interesting.

Also, in this paper the subjects are mostly RR, but they have EDSS scores. Does that mean their EDSS scores are based on their debility during relapses? Does one have to be basically asymptomatic during remissions in order to be termed RRMS?
I dont have MS, but I study all diseases of immune activation. I had severe CFS and am 95% well, 1 yr into antimicrobial treatment.
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Postby mrhodes40 » Sat Nov 19, 2005 2:24 pm

Hi Eric!
What a great mind you have.

As for the CPn in MS brains, there have been many studiies from the ludicrous (We looked at pw MS and OND controls. IgG antibodies to CPn in both groups was similar. We conclude Cpn has nothing to do with MS) to the careful and thorough. I am not aware of any research showing t-Cell studies in the MS brain for CPn This one however used many methodes to determine presence of the organism: http://www.CPn Help.org/?q=node/137. It is also not uncommon for oligoclonal banding to be checked for CPn sensitivity also See this here: http://www.CPn Help.org/pdfs/MS-Oligoclonal.pdf

In this paper presence of gene transcription and heat shock proteins was also noted in the CSF of MS patients.http://www.CPn Help.org/pdfs/cpncsfofMS.pdf

The physicians links on the CPn Help site is what you want to read. We have the whole techinical citations of several key works posted on that page of the site.

The EDSS is a score of a MS patient's ability to walk between exacerbation; Their base ability. The level of non functionality during one is temporary and not representative of recovery. Some people have huge losses of function and recover completely, others may have a smaller loss and recover not at all.
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Postby LifeontheIce » Sun Nov 20, 2005 6:38 am

I don't think Tovaxin is doing anything to cpn. It removes T-cells that damage myelin, stopping the clinical progress of the disease.
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Postby EricJohnson » Sun Nov 20, 2005 4:11 pm

I havent tried to understand the Hellings & van der Aa data myself... and I dont have any idea whether they used an optimal protocol for the treatment, or whether they might have some sort of agenda for/against the treatment.

But I can report that their paper says:

In conclusion, we demonstrated a significant immunological response both to the vaccine cells (anti-idiotypic) as well as to activated cells in general (antiergotypic) [...]


I am not sure whether they think the antiergotypic response is large and lasting enough to be of clinical significance. They dont seem to say clearly(?). However, if it is large and lasting enough, it does seem like it could reduce T-cell mediated inflammation provoked by chlamydial antigens (or any other auto- or allo-antigens of any kind).

Again, I'm kind of a dabbler in this particular subject. So one might want to get someone elses opinion on this; mine is rather superficial.
I dont have MS, but I study all diseases of immune activation. I had severe CFS and am 95% well, 1 yr into antimicrobial treatment.
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