O.K., I guess I am going to keep this thread up to date with information I find that supports the hypothesis that MS is a due to a regulatory T-cell defect.
This theory could be wrong, but I believe there is a lot of information to support this and it seems like this forum is the best place I have found to share ideas.
So, to answer Jimmylegs question, I do not monitor my magnesium levels, but I do eat a lot of nuts which are supposed to contain a lot of magnesium.
Now back to the subject at hand.
Here is another recent study that evaluates Regulatory T-cells in the Theiler's virus mouse model of MS. For those not familiar with this model it is not EAE, but is induced by a virus instead of an auto-antigen:
And the conclusions:
"In summary, our findings strongly indicate that differences in
the numbers and the ratio of CNS T effector:Treg cells during acute
TMEV infection control the efficiency of the anti-viral immune
response resulting in virus persistence and resulting long-lasting
effects leading to the eventual development and progression of the
autoimmune demyelinating disease. The preferential expansion of
Tregs in TMEV-infected SJL/J mice, as compared to disease-resistant
C57BL/6 mice, suggests the possibility that genetic susceptibility to
certain autoimmune diseases may be in some instances due to
‘regulatory mimicry’. This would encompass a situation wherein
a clonotype of nTregs expressing a self antigen-specific T cell
receptor selected on particular MHC backgrounds could be activated
to expand in response to a cross-reactive epitope expressed
on an infectious agent. This expanded population of Tregs would
then ameliorate or delay the clearance of the infectious agent in the
target organ of the autoimmune disease setting the stage for
promotion of the development of autoimmunity via mechanisms
such as molecular mimicry or epitope spreading. These findings
thus have important implications to our thinking about the
potential mechanisms underlying induction of human autoimmune
disease secondary to virus infection."
My takeaway is that this is further evidence that MS may be initiated by a viral infection which causes an inappropriate immune response that is not halted by self-tolerance due to a defect in the natural regulatory T-cell (nTreg) function.