Visit the Microscopic Colitis Foundation Website
Thanks to Linda, for inspiring me to think about this topic a bit more, so that I can offer a much better argument against an overactive immune system, as a potential cause of MC. Of course, the arguments that I offered in my previous posts about this topic, still stand, also. Bear in mind that this is strictly my opinion, and it is not chiseled in stone.
Anyway, the point is, when you think about it a bit, it's pretty obvious that we, (and the medical community), have been missing the point here. We all know that MC, (and the other IBDs), are basically T-cell reactions, (at least this is how they begin). For some arbitrary, (and probably incorrect), reason, we've just assumed that IBDs, (and in fact, all autoimmune diseases), are a result of an overactive immune system, that produces too many T-cells, (natural killer T-cells). Why would we assume that, when the problem could just as easily be an underactive, (or compromised), immune system, that produces too few regulatory T-cells, (suppressor T-cells)? Of course, part of the problem may be that natural killer T-cells are old knowledge, whereas regulatory T-cells are relatively new knowledge, and mainstream medical thinking is usually very resistant to change, when it comes to long-term established principles.
Consider the current thinking regarding the mechanism by which it is thought that LDN works for treating MS:
http://www.msrc.co.uk/index.cfm/fuseact ... pageid/651Contrary to the common belief that MS is due to over-activity of the immune system, MS actually occurs due to a reduction in immune system activity. Specifically, it is the reduction in number of the suppressor T-cells within the immune system that permits the damaging CD4, helper T-cells to do their harm. Thus, during an acute relapse, the overall number of T-cells is reduced, the normal balance of helper T-cells and suppressor T-cells is disrupted and the CD-4, helper, T-cells tend to predominate. This is the situation most pronounced during an acute relapse but a similar situation occurs, perhaps to a lesser extent, in chronic progressive MS.
Under the influence of LDN it has been demonstrated that the numbers of T-cells may increase by more than 300%. Thus, when the number of T-cells is initially increased, the overall predominance of CD4, helper T-cells, at this time, will expectedly increase the intensity of the MS, therefore temporarily increasing some symptoms.
As the number of T-cells continues to increase, the normal balance of suppressor to helper T-cells is restored, the activity and intensity of the disease process is reduced, and symptoms once again diminish and improve.
Well, if "renegade" LDN researchers are aware of this, why isn't it even on the radar of mainstream medicine? Why does the establishment blindly continue to accept obsolete assumptions as fact, even when they obviously contradict real world events? Surely, in this day and age, most researchers dealing with issues that relate to the immune system, are well aware of the role that regulatory T-cells play in so-called autoimmune diseases, (at least they should be).
For those unfamiliar with this aspect of the immune system, regulatory T-cells (sometimes known as suppressor T-cells). are a specialized form of T-cells that act to suppress activation of the immune system, and thereby maintain immune system homeostasis and tolerance to self-antigens. For many years, there was a lot of controversy among immunologtists, over whether a dedicated population of suppressor T-cells even existed. Recent advances in the understanding of the characteristics of these cells, however, have firmly established their existence, and their critical role in the performance of our immune system. In fact, experiments with mice have demonstrated that the immunosuppressive potential of these cells can be harnessed therapeutically, to treat autoimmune diseases, and to facilitate the transplantation of tolerance, or to specifically eliminate tolerance, so that regulatory T-cells might be used to protect against cancer.
Obviously, in order to function properly, the immune system must discriminate between self and non-self, because when self/non-self discrimination fails, the immune system destroys cells and tissues of the body, and as a result, causes what is known as autoimmune disease. Regulatory T cells actively suppress activation of the immune system and prevent reactions against self, IOW, autoimmune disease.
Everyone here, who has MC, saw their disease develop either during, or immediately following a period of events that are well known to suppress the effectiveness of the immune system. We are all familiar with those "events", because they are frequently listed in the literature about MC, as "causes of MC", or "events leading up to the development of MC". Whatever they are called, they all have one thing in common - they all cause the immune system to be either suppressed, or compromised, or both.
So I'll say it again - I don't believe that MC is caused by an overactive immune system, (and I know that I'm not the only one here who feels that way). I believe that it is caused by an underactive, (compromised), immune system, that probably doesn't produce enough suppressor T-cells. Just because it's possible to treat the disease by suppressing the immune system, does not prove that the immune system is overactive, (that assumption is where many "experts" go wrong), it simply means that part of it is still working, and part of it is compromised. I assume that most immune system experts know all this, but for some reason or other, they still cling to the incorrect assumption that an overactive immune system is the problem. Clearly, it is not.
Tex
