Guest guest Posted August 8, 2010 Report Share Posted August 8, 2010 Apparently, there are at least two types of MS - one gamma-interferon sensitive and the other tied to IL-17. If you are the gamma-interferon-sensitive type, then beta-seron may be right on target for you. Apparently, the same researchers will be revealing where Copaxone fits in as well in the future . . . and they will likely patent a lab blood test to determine which type you are. Encouraging stuff. I may give beta-seron a try to see in a crude test which type I am . . . I take Copaxone now. Cheers, Two cytokines called gamma-interferon and IL-17, for example, tend to induce the kinds of inflammatory immune-system arousal that can trigger multiple sclerosis. Axtell (now a postdoctoral scholar in Steinman's lab), Steinman and their colleagues were able to induce two superficially similar forms of EAE in mice by directing the myelin-attacking T cells to predominantly secrete either gamma-interferon or IL-17, respectively. The researchers found that beta-interferon improved the condition of animals whose EAE had been induced by gamma-interferon-secreting T cells, but exacerbated symptoms in those whose EAE had been induced by IL-17-secreting T cells. Intrigued, the investigators turned to humans. Another postdoctoral scholar in the Steinman lab, Brigit deJong, MD, the study's second author, had previously been involved in research in Amsterdam in which multiple-sclerosis patients were treated with beta-interferon and meticulously followed up. The Stanford group obtained blood samples taken from 26 of these patients both before and about two years after the initiation of treatment. Without knowing which samples came from patients who had responded well or poorly to beta-interferon treatment, they went about measuring IL-17 levels in those samples. Eventually, patients' follow-up histories were revealed to the researchers and their measured IL-17 levels were paired with their post-treatment progress. A clear pattern emerged. Measurements of a particular variety of IL-17, called IL-17F, clustered at either very high or very low levels in individual patients' blood. Those with very low detectable blood levels of IL-17F responded well to beta-interferon treatment, experiencing no relapses or instances of required steroids (to quickly shut down a malfunctioning immune system). But patients with very high IL-17F levels — about one out of three subjects — responded poorly by the same criteria. In fact, said Steinman, there is some evidence that beta-interferon actually worsened these patients' conditions. Quote Link to comment Share on other sites More sharing options...
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