Multiple forms of MS?
One of the many puzzling and infuriating aspects of multiple sclerosis is that the disease follows such different courses in different people. On top of that, people's responses to the handful of drugs that can slow the progress of MS vary widely. Some patients find their symptoms diminish quickly once they start drug therapy, while others cast about for years in search of a drug that does them any good at all.
Researchers at Stanford University may have discovered why that is. It turns out there may be two different forms of MS, and each may respond differently to drug treatment.
Their work built on a discovery (by the lead author when he was a grad student at the University of Alabama) that one of the major MS drug therapies, beta-interferon, can reverse paralysis in mice in which an animal model of MS (called experimental autoimmune encephalitis, or EAE) had been induced. Beta-interferon (marketed as Betaseron) was known to have the same effect in some humans.
Then, at Stanford, researchers led by Lawrence Steinman found they could induce EAE in two different ways, each using a different cytokine, or immune-system signal chemical, to trigger the damaging autoimmune response characteristic of the disease. The cytokines they used were called gamma-interferon and IL-17.
Steinman's team learned that mice whose EAE was triggered by immune cells that secrete gamma-interferon responded positively to beta-interferon. But in those whose EAE was triggered by IL-17, disease symptoms were actually exacerbated.
To see if the same might be true among humans with MS, the team analyzed data collected in an Amsterdam study for a group of 26 people who had been treated with beta-interferon. When the team matched blood samples to data showing how well or poorly each patient had responded to the drug, they saw a clear pattern. Those whose blood had high levels of a variety of IL-17 (called IL-17F) had responded poorly to the drug, while those with low levels of that cytokine responded well.
Why is this important? If that finding holds true in other lab work and in larger human studies, people with MS might be able to determine whether they're likely to respond to a drug therapy by taking a simple blood test. That would save them the time, money and frustration of dallying with an expensive drug that's ultimately not going to help. (Beta-interferon, according to the study, only benefits about half the people who try it.) Steinman is now investigating whether the phenomenon occurs with other MS drugs.
It's also important because it's clear that MS is a disease to be chipped away at, not understood all at once through some single Eureka! discovery. Every little (or big) thing we learn about this confounding disease gets us that much closer to cracking it once and for all.
Folks with MS, how many treatments have you tried? How has your disease responded to them? Please share your experiences in the Comments section.
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