Why do relapses go?

Frank · Posted: Tue Mar 13, 2007 1:38 pm Post subject: Why do relapses go?

Hi,

I recently wondered how it could be possible, following the traditional autoimmune theory, that the immune system comes to the point where it attacks the mylin sheath and after some time/event it calms down and stays quiet until the next relapse.

As far as I know, if the immunesystem comes across an "enemy" structure the immune-cascade is going on as strong as necessary, until the enemy structure is completly removed (or at least no longer detctable to the immune system - like a latent virus).
Off course the immune-system does have are anti-inflamatory mechanisms, but these should not halt the attack until the job is done.

So in MS, when it attacks the mylin I would expect a heavey reaction that leads to the "complete" eradication of mylin at a single blow.

Does anyone of you have a conclusive idea how it comes that relapses pass off?

Thanks

--Frank
_________________
Current regime: Tysabri restarted 05/2008 after LDN, ABX Wheldon Regime for 1 year, interested in T-Cell vaccination, helminth immunomodulation

NHE · Volunteer Moderator Joined: Nov 21, 2004 Posts: 777

Hi Frank,
That's a good question. I hope that this reply helps to answer it. From MRI studies, it has been shown that not all lesion activity produces clinical symptoms. For a graph depicting this process, please see page 6 of this document.
http://www.msu.edu/~lyonro/Opexa06.pdf

NHE

Frank · Posted: Tue Mar 13, 2007 4:01 pm Post subject:

NHE, thanks for answering.
I took a look at the presentation from your link and I do understand the content of the mentioned graph.

But my point is that there is a break of the immune-systems attack, isnt it?
If that would not be case, then inflamation markers in blood like CRP or T-Cell count etc. must be elevated all the time, which does not happen to be, does it?

And in case of a continuous inflamation I would MS expect to worsen much more dramatic, not some accumulated disability over years.
For example I would compare tissue rejections after organ transplantation which are indeed rapid.

So how could a break make sense, regarding, that the targeted antigen (myelin) is still present?

--Frank
_________________
Current regime: Tysabri restarted 05/2008 after LDN, ABX Wheldon Regime for 1 year, interested in T-Cell vaccination, helminth immunomodulation

CureOrBust · Posted: Wed Mar 14, 2007 2:33 am Post subject:

Lets not forget there is a another step in the MS disease process. The errant immune system has to be let into the CNS, through a BBB. Steroids are normally used to stop attacks in their tracks, and one of their modes of actions has been found to be in closing the BBB.

If we assume the immune system continues to be myelin reactive, the BBB may somehow change to stop letting it in. Then the question becomes what triggers this change.

Frank · Posted: Wed Mar 14, 2007 4:40 am Post subject:

I quote a discussion between Chris and Lyon on that subject:

Frank · Posted: Wed Mar 14, 2007 4:59 am Post subject:

I just wanted to add this link to the discussion. It is mostly about how B-Cells mediate through BBB:

Determinants of Human B Cell Migration Across Brain Endothelial Cells
The Journal of Immunology, 2003, 170: 4497-4505.

--Frank
_________________
Current regime: Tysabri restarted 05/2008 after LDN, ABX Wheldon Regime for 1 year, interested in T-Cell vaccination, helminth immunomodulation