Hello everyone,
I wanted to add my view on the basic statements of the autoimmune theory:
I refer to an explanation given for on various locations and for example here:
UCSF Multiple Sclerosis Center FAQ section "The Role of the Immune Systems"
My strongest objection is, that the basic statements of that theory are far too vague to only follow this track. Autoimmunity argues that:
An unknown pathogen (a virus or bacteria) causes T-Cells to go in an active state. Some of these activated T-Cells cross the BBB.
In the referenced model they do not say there is anything wrong with the permeabiliy of BBB but it is considerd as a usual process that T-Cells can cross BBB.
Why do they get to the CNS at all? Is there something wrong in this location? T-Cells have to be guided in some way to reach their designated target.
After entering the CNS coincidently?! they are reactivated by microglia which present mylin peptides on their MHC; to the T-Cells this peptide looks somehow the same as the pathogen that originally activated them.
This causes the T-Cells to attack the myelin sheath.
The only thing I know that has been evidently found so far are tissue samples which contain different types of immune cells.
Thats not really convincing, and certainly does not justify to leave other models aside.
I'm sure all of you know the 2004 austalien study
at ThisIsMS
by Dr. Barnet who found, that in some (the earleies state?) lesions oligodendrocyt death occured while immune-cells were abscent.
So even this one thing autoimmunity had, could be seen in a different light.
In addition, autologous stem cell transplant is evident not to stop disease progression (at least in late states of MS) and there are still new lesions forming within the CNS but with only very few immune cells on-site.
On the other hand many studies found significant increased virus (e.g. HHV-6) and bactia load in different samples (Blood, serum, CSF) - references can be added if someone is interested in.
The only one human clinical trial I could find that targets virus in MS used valacyclovir to fight HHV-6:
pubmed
It did not find statisticly significant difference between placebo and verum.
Thats not too surprising, as this study states acyclovir is not potent to fight HHV-6 infection in glia cells. Its somehow frustrating they didnt even take the time to evaluate what drug to choose:
pubmed
From my personal point of view, a secondary immunesystem involvement, as garbage collector, after some pathogen causes cell death in the CNS seem pretty rational, while the classic autoimmune approach lacks a continuous concept, especially at the beginning of the theory.
At least it would be reasonable to have some serious efforts on the infections in MS. Potential drugs would be available and do only cost a fractional amount of standart MS regimes.
Another important point about autoimmunity I find hard to explain, is described in this thread:
ThisIsMS Thread: Why do relpases go
Its basic question is: Why would the immune-system stop its attack if the pathogen (Mylin) is still present.
Maybe the threads title was not the best wording
.
Greets
--Frank