
Proliferation of both freshly isolated CD4+ T cells and MBP-specific T cells was significantly inhibited by 1,25(OH)(2)D(3). Moreover, activated Vitamin D enhanced the development of IL-10 producing cells, and reduced the number of IL-6 and IL-17 secreting cells
that's reason enough right there to not do the MP; 1,25D is not acting like a steroid, it is slowing down the parts of the immune system that need slowing down in MS....and increasing the parts that need increasing.
Now if an MPer was here they would tell an elaborate story about how this does not count because it was done in a lab dish, as if fresh blood behavior in a lab dish is completely different than in the body.
they would point to this section as support for themselves though
What that says is that the t cells turned 25D into 1,25d, they have been claiming this is because the germs are making this happen. In fact activated macrophages can convert 25d to 1,25d in a local area like that, that is known. But that does not result in overall high 1,25d as the other papers show and it also is not a bad thing for the 1,25d to be there as it modultes the immune system in a very positive way for MS.Interestingly, T cells were able to metabolize 25(OH)D(3) into biologically active 1,25(OH)(2)D(3), since T cells express alpha1-hydroxylase constitutively
this little bit
is important because note that the VDR was activated no problem by the 1,25d. This is another aspect of vitamin D activity the MPers say is not working in MS because the VDR, they say, is inactivated by 25d. No evidence of that either.Notably, Vitamin D receptor expression was induced by 1,25(OH)(2)D(3) in both activated and resting cell
All in all I hope pwMS who are considering this marshall protocol learn what they say over there then read this thread. Many people who never studied the MP will find this information a little confusing, but to those who already drank the koolaide, the more detailed infor will be welcome.