1 he told me only 10% of patients were testing out positive for MRTC's-but this was early on. What is that number known to be now?
Unless he is on the scientific advisory board, he would not have that information. If you think he is correct, you should ask him for the specific source of his information. Tell him you have heard figures different than his.
I have not heard any figures. Remember it is good news to be in the study and not have detectable MRTCs. In the redose study of the people that Zhang treated in the late 1990s, I believe 2 out of 12 were no longer producing MRTCs, and that was after a 6-year absence from treatment.
2 if those of us like me want to know just for our own sake if we make MRTC's so we can wait for it, can we be tested??
I don't think so. I don't know if the FDA would have to approve a test to detect MRTCs, but even if they didn't, Opexa is the only company with an analysis that determines MRTCs using 163 different peptide fragments over 3 of the major myelin proteins to identify an individual’s MRTC set. The group in Israel uses 2 of the major proteins, and I don't know how many peptides.
Just curious; Copaxone was designed to look like myelin and divert the immune system. It does not work that way, but I wonder if people who took it are more likely to have MRTC's
I don't even have a guess about that, but I will ask. If there is something to that idea, I will post what I find out, but it will only be someone's speculation, an educated speculation.
I would like to know because if it is true that I DO have them, this might cause me to make sure that decisions I make now are designed to take advantage of that later when it is out. For example, I have RA and can get Rituxan if I want it. That depletes B-cells. If I added Tovaxin to that later that might be a comprehensive approach.
The B-Cells that are causing RA are activated by a trigger different from MS. Rheumatoid Arthritis is also an autoimmune disease. I believe the destruction in RA occurs in the synovial tissue that lines the joints and produces synovial fluid. Synovial fluid nourishes and lubricates the cartilage and bone in the joint. I have not spent much time looking at RA other than knowing that it is an autoimmune disease.
Since Opexa already has a vaccine for RA that had a successful phase I/II trial in China, T-Cells must also play a role in RA. Since there is no blood brain barrier issue to affect the mechanics of the disease, RA may prove to be far more complex than MS. Lupus is another autoimmune disease where B-Cells are the primary problem.
Even though I think that B-Cells might play some role in MS, it appears that the T-Cells are the destructive force attacking myelin. The immune system is a system and the T-cell may be the primary problem, but it is possible that some other component of the immune system is also at work in MS. I hope that Tovaxin can control the T-Cells, eliminate the attacks, and if there is another cell evolved in MS, scientists will be able to more easily identify it.
But if on the other hand I do not have them at all, then I can forget about it and do whatever treatment seems good to me, possibly Revimmune.
If I were going to speculate on what treatment would be the best adjunct to Tovaxin, it would be Tysabri. I hate to say that, but the mechanism of Tysabri is such that it does not allow any of the T-Cells to cross the BBB, which would make them an easy target for Tovaxin. I don't know which treatment would come first or if they would be done at the same time.
My 99½ -year old Grandmother passed away this week. Both the Chicago Tribune and Daily Herald did an article on her, Mary Klein. I will miss her. I am heading home tomorrow and will probably check back in a month from now to see how the 100 plus days club thread is doing.