THe Barnett and Prineas paper is my favorite. I was leaning in the way of "MS is not AI" before that but when that paper came out overnight I was completely convinced. If you read it and understand it, it shows that MS CAN"T be AI...although the Luccinetti camp tried to argue that the fact the person had died somehow stopped the immune system from being there in the normal way.................uh that doesn't work though
ALso
HERE is a paper that compares EAE to MS and shows very plainly why these are not at all similar on a cytokine level. Since EAE is a AI disease, this is problematic if MS is not showing with the same type of cellular activation.
Second
Quote:
Some see MS as a T-cell-driven autoimmune inflammatory disease, targeting the myelin sheaths in the central nervous system,3 but there is no proof.
People who believe that AI model ignore this fact and explain it away with a lot of talk about how complex MS is, how difficult to work with, etc. Really they take it on faith that MS is AI because they believe it. SO it is AI because they believe it is AI not because it is proven to be.
But the bottom line fact is that for a disease to be autoimmune it has to have a "PRIMED" immune system, there has to be an antigen in the body that the immune system has been programmed to attack, even though it is healthy...and it has to go to this healthy area and start breaking down perfectly healthy, perfectly functional cells that express that antigen and otherwise would have been working correctly had they been left alone.
The lab is good at finding these kinds of cells we have identified them over and over in all kinds of diseases like rheumatic fever. They've looked for 60 years and can't find one in MS. The fact they can't find this cell in MS is damning for the theory that it is autoimmune.
If the immune cells are going there because the tissue is hurt and damaged, it is not autoimmune. Period. The cure, in that case, is to stop the hurting a damaging from happening in the first place.
I don't know if CCSVI is the cause of this damage that brings the immune system in or not, but it sure is a decent candidate...............
considering the same problem CVI in legs causes cell damage and destruction in that leg that looks just like an MS lesion from a cellular standpoint as shown in this table comparing MS and stasis ulcers both have these same features(the numbers are references). From Zamboni '06 Big Idea
Quote:
Perivenous inflammation + 2,4,5,9,10 + 17–25
erythrocyte extra-vasation + 4–9 + 18–21,24
Haemosiderin deposits + 4–9 + 20,21
Adhesion molecules and white cells activation+ 10–12 + 26,27
Macrophage migration-infiltration + 4–6,12 + 26,27,30
T cell migration-infiltration + 12 + 26,27,30
Iron laden-macrophage + 4–6 + 20,21
MMPs hyper-activation + 4–7,15 + 30
TIMPs hypo-expression + 4–7,15 + 30
Local iron overload + 4–9 + 18,20,21,28
Urine haemosiderin test + 9 + Personal unpublished
data
HFE mutation + 5,6 + 29
Fibrin cuff (on going reparative process)
I've said it before but it bears repeating that these immune cells listed above are seen as proof MS is autoimmune..........but these same cells are there in leg ucers in order to clean up the hurt and amaged cells, so how does that compute?
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, but your keeping on connecting dots and making corralaries (sp?) is just incredible to me. I love you guys, you are the best.
