Autoreactive T-Cell Generation (hypothesis)

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Autoreactive T-Cell Generation (hypothesis)

Postby CureOrBust » Wed Sep 13, 2006 3:47 am

Although, not MS specific, and I am reading into it things the hypothesis isnt aiming for...

... results in too few T cells, and the body tries to correct this by inducing a vigorous expansion of the remaining T cells, creating a more autoreactive population.

http://www.scienceagogo.com/news/20040315203720data_trunc_sys.shtml

I read this as another theory of how our immune cells become auto-reactive.
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Postby Lyon » Mon Sep 25, 2006 7:20 pm

oo
Last edited by Lyon on Sat May 07, 2011 8:44 am, edited 1 time in total.
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Postby Brainteaser » Mon Sep 25, 2006 11:11 pm

This theory is quite good and I have heard it before. But does it explain the latitudinal pattern of MS? Are Tasmanians 'cleanlier' than Queenslanders, Canadians/Americans, Scots/English etc?
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Re: Autoreactive T-Cell Generation (hypothesis)

Postby NHE » Tue Sep 26, 2006 1:37 am

Lyon wrote:I wonder how it's progressed in the time since.

You could always try searching for articles by the same group of researchers. Another option is to use a citation index to search for articles which have referenced this one. Note that your local library may have access to a citation index, if not, then if you have a university near you then their library will surely have one available (a community college may also have one but it could be less likely).

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Postby bromley » Tue Sep 26, 2006 2:31 am

Dear all,

This hygiene theory has been around for some time. EBV has been suggested as a possible cause / trigger for MS. Some research shows that getting infected with EBV (mono / glandular fever) later in life (late teens) puts you at higher risk of getting MS. In Africa, children tend to be exposed to viruses such as EBV at a much younger age and MS is almost unknown.

One of my neuros, Dr Coles, is presenting at an MS seminar in November. One of the topics he is presenting on is 'the role of EBV and deficient regulatory cells'.

The importance of regulatory cells (Killer T Cells) also seems to have a key role. The Dacluzimab trial showed that the drug increased killer T cells and this had benefit. Results from the Dacluzimab trial are being presented at the ECTRIMS conference this week.


http://www.thisisms.com/article261.html

Of course this does not explain the gender difference or the vit D influence.

Ian
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Postby CureOrBust » Tue Sep 26, 2006 3:59 am

I personally think the hygiene angle confuses the peice of info that was new to me, and the info I was trying to share. This point of interest being the way the immune system (in particular the T-cells) is generated.
... Often people with autoimmune diseases like Type 1 diabetes, lupus, and rheumatoid arthritis have low T cell numbers.

If the body detects low levels of T cells, it resorts to homeostatic expansion, a mechanism that has never been associated with autoimmunity before. Under homeostatic expansion, growth signals stimulate the existing T cells in the body to divide and multiply....

I personally find it interesting that their theory is that if the T-cells are generated by cell division (homeostatic expansion), instead of the "normal" method (whatever that is) there will be autoimmunity.

Here is a PubMed reference that sticks to the point, that was new to me.
During illness and stress, the immune system can suffer a considerable loss of T cells (lymphopenia). The remaining T cells undergo vigorous compensatory expansion, known as homeostatic proliferation, to reconstitute the immune system. Interestingly, human diseases of autoimmune etiology often present with immune deficiencies such as lymphopenia.


If these guys were 100% correct, treatments could be based around drugs that stopped homeostatic growth, and pushed the normal method. if these guys were only 30% correct, they could match our current treatments. And thats what caught my eye.
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Postby raven » Tue Sep 26, 2006 8:27 am

Perversly it seems that in MS patients the homeostatic mechanism of T cell proliferation fails. This has been seen in studies of patients who have been treated with Campath.

<shortened url>

I have the full paper of this as it was given to me by one of the researchers. It makes interesting reading.

Although as it has been observed in patients post treatment (no way to do it otherwise) the old cause and effect problem kicks in i.e. was the failure there before Campath or has it been caused by treatment. Perhaps this effect upon the homeostatic mechanism is in part responsible for the effectiveness of Campath...

Questions, questions.... Very few answers... :(

Robin
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Postby Lyon » Tue Sep 26, 2006 12:32 pm

oo
Last edited by Lyon on Sat May 07, 2011 8:47 am, edited 1 time in total.
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Postby Lyon » Tue Sep 26, 2006 1:16 pm

oo
Last edited by Lyon on Sat May 07, 2011 8:46 am, edited 1 time in total.
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Postby scoobyjude » Tue Sep 26, 2006 5:20 pm

Bob, did you ever organize your site about helminth therapy? Remember, once you prove it works, I'll be the first in line to ingest one of those buggers :lol:
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