By Val Willingham

CNN Medical Producer

Scientists and doctors who study multiple sclerosis know, as of now, one of the best way to treat the condition is with beta-interferon. But over the years, the drug's effectiveness has been lukewarm in some people causing a third of all MS patients who are on the drug to suffer from uncomfortable flu-like side effects. Many can't handle it and so far, researchers have never figured out why.

Now scientists from Stanford University School of Medicine may have discovered that there are actually two kinds of multiple sclerosis and that each reacts differently to the standard treatment.

Researchers know multiple sclerosis is triggered when immune cells, called T cells, attack the myelin sheathing, which insulates neurons in the body. Healthy myelin sheathing is essential for the nervous system to function properly. When this material is attacked, it can cause serious symptoms including paralysis and blindness in those with MS.

In this study, published in the current issue of Nature Medicine, researchers established animal models of multiple sclerosis by injecting mice with myelin into their immune systems, causing it to attack the animals' own myelin nerve-cell coatings, much as MS attacks a human being’s. By looking at these animals and treating them with beta-interferon and then testing their blood the researcher found there were actually two different types of MS, caused by different patterns of T cells in the body. So what works for one, doesn't necessarily work for the other.

The researchers found that beta-interferon improved the condition of animals who had MS caused by gamma-interferon-secreting T cells, but made the symptoms worse in those mice whose MS was caused by IL-17-secreting T cells.

Intrigued, the investigators turned to humans. One of the study's authors, Dr. Brigit deJong, had previously been involved in research in Amsterdam in which multiple sclerosis patients were treated with beta-interferon and closely followed. The Stanford group obtained blood samples taken from 26 of these patients both before and about two years after the initial 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. The human results were much like the animal models. Those with high amounts of IL-17 T cells had had negative reactions to beta-interferon.

"By making these distinctions in large human studies, people with multiple sclerosis might someday be able to take a simple blood test to see whether they are likely to respond to treatment with the standard multiple-sclerosis therapy." says senior study author Lawrence Steinman, M.D. of the Neurology and Neurological Sciences Department at the Stanford University School of Medicine,

If an inexpensive test can be developed to detect IL-17 in humans, MS patients and their doctors will know whether beta interferon is or isn't going to work. "For those who don't have the IL-17 T cells," notes Steinman, "those patients can receive beta-interferon and probably not in a diluted form but in a higher dose, which will help them better fight their illness."

According to the National Multiple Sclerosis Society MS affects 400,000 people in the United States. Dr. Patricia A. O'Looney, vice president of biomedical research for the National Multiple Sclerosis Society, says the new research is very exciting. "Obviously this will need more testing in human subjects," explains O’Looney, "But this is a positive step in the right direction to helping to treat MS and other autoimmune conditions."

Editor's Note: Medical news is a popular but sensitive subject rooted in science. We receive many comments on this blog each day; not all are posted. Our hope is that much will be learned from the sharing of useful information and personal experiences based on the medical and health topics of the blog. We encourage you to focus your comments on those medical and health topics and we appreciate your input. Thank you for your participation.