Regulation of the immune system may be part of the pathogenesis of relapsing-remitting MS (RRMS). In this study, the investigators demonstrate a dichotomy within the frequency of a regulatory white blood, cells called T-regs, among newly diagnosed RRMS MSers but not in healthy controls. A group of RRMS MSers was characterized by a significantly lower percentage of T-reg cells than that of their matched, healthy controls, and this was inversely correlated with their score on the EDSS. Since the EDSS reflected severity of the last attack, this study demonstrates a correlation between low frequency of T-reg cells and severity of clinical disease in RRMS.
We have discussed what Th1 and Th2 T cells are in the past. For many years immunologists thought that the immune response was controlled by T suppressor cells, anergy, then Th2 and now the flavourof the month, or should I say years, are the T regulatory or T-reg cells. These cells are thought to prevent autoimmunity from occuring. These express a number of markers such as FoxP3 and CD25, which is the interleukin-2 receptor (which controls T cell growth). This study suggests that the healther the MSer is the less number of Tregs there are and so fits with dogma. If they could be induced then the idea is that it will inhibit disease. This is the mechanisms that most animal studies now show as a working mechanism…it wouldn’t be dogma if people were not like lemmings and all find the same thing :-).
Daclizumab, a drug in phase 3 development for MS, blocks the action of CD25 as so you might think it would block T-reg function and make MS worse, but it appears to inhibit relapsing MS so quite the opposite. However, daclizumab’s action appears to have nothing to do with T-regs and more to do with blocking the activation of T cells. Other mechanism may be by activating and expanding the numbers of the so called natural killer cells; these cells are important in fighting infections. Despite all these theories daclizumab appears to be effective in treating relapsing MS.