George,
Yes, I read that article and it sheds a lot of light on the fact that the same T-cells were tracked during an attack which to me shows that epitope spreading could indeed be a factor in MS.
Incidentally, I see a neurologist who is a professor at the school of neurology at Wayne State University Medical School and is an expert on ADEM which is what I have. This disease is essentially EAE in humans. One day I went to the hospital with vomiting, fever, a headache and double vision. 30 days later I was released with an EDSS score of 7 in which I was totally imobile from the waist down.
About 1/3 of people with ADEM go on to have reacurrences and are eventually diagnosed with MS (which appears to be my case).
So, I my mind there is no question that MS is autoimune.
Which leads me to a new article about the "Biography" theory of MS, otherwise known as the "Darwinian Medicine" hypothesis:
http://www.hindawi.com/journals/ad/2011/708750/
Quote:
Attention has recently focused on environmental factors associated with the increase in the incidence of several classes of disease in the industrially developed nations. The concept, forming the basis of the emerging discipline of “Darwinian medicine” [58], is that hygiene-related factors isolate the human population from micro-organisms, both pathogens and, probably more importantly, commensals, that are crucial to the establishment of beneficial immunoregulatory networks. Thus, in principle, an “interkingdom cross-talk” between microbes and the human host can establish patterns of immune reactivity that prevent various allergic, autoimmune, and inflammatory diseases while a failure of such cross-talk can facilitate them [59]. One consequence of improved hygiene is that certain infections that were previously regularly encountered in infancy now occur at a much later time in life and after other infections may have altered the patterns of immune responsiveness. Infection by EBV is a good example, and it has been postulated that various other infections acquired before EBV may affect immunoregulatory networks, thereby leading to an attrition or eclipse of those regulatory T cells (Tregs) that would otherwise protect against MS [10]. In this context, Tregs, though essential to immune function, may in some circumstances induce harmful effects and have therefore been termed a “dangerous necessity” [60].
Accordingly, a critical determinant of MS risk could be a compromised number or activity of protective Tregs [61, 62]. During an active and specific T cell-mediated immune response there could well be a competition with other kinds of T cells, most likely T-helper-cells, recognising the same epitope as the Tregs or epitopes closely spatially situated on the relevant antigen(s). As a consequence certain T-helper cell populations, that induce production of specific antibody, could become expanded and, thus, account for the diverse rise in antibody levels as epiphenomena with little or no pathologic importance. Notwithstanding, the local production of measles, varicella, or rubella-specific antibodies in the central nervous system can be useful for diagnosis [28–30], and the production of anti-HERV antibodies may become of use as prognostic factor for MS disease [4, 63].
To me, I think this theory explains a lot such as the influence of viruses (hygeine theory) on the development of the immune system. The Treg/Teffector cell balance seems to play a role and this "biolgraphy" of the immune system would explain why twins seem to have the same genetic make-up but different suseptability to acquiring MS. Also since Vitamin D also appears to promote the development of Tregs, I think the answer to the question is near.
Keep the research comming!
Login
Register
FAQ
Search
