Two drugs that help multiple sclerosis patients might be even more powerful in combination, according to a report presented at the American Neurological Association's 126th annual meeting, September 30 to October 3 in Chicago.
American Neurological Association (ANA)
CHICAGO --Two drugs that help multiple sclerosis patients might be even more powerful in combination, according to a report presented at the American Neurological Association's 126th annual meeting, September 30 to October 3 in Chicago. Researchers from Sweden, have determined that the two drugs, interferon-beta (IFN-beta) and glatiramer acetate (GA, also called copolymer 1 or Copaxone) exert their beneficial effects by acting on the same class of immune system cells, but by different mechanisms.
"This suggests that we should try a long-term clinical trial comparing IFN-beta or GA alone, versus the two in combination," said lead author Yu-Min Huang, M.D., Ph.D., of the Karolinska Institute in Stockholm, Sweden.
Multiple sclerosis (MS) is a disorder of the nerve fibers of the brain and spinal cord. In MS patients, scarring (sclerosis) replaces myelin, a substance that normally insulates the nerves and speeds electrical conduction through the fibers.
Depending on which nerve fibers are hindered, patients can experience problems ranging from weakness and clumsiness to numbness, visual disturbances, and even emotional and intellectual changes. Some patients experience MS as cycles of relapse and remission; others progress to severe debilitation and may die from the disease.
Though the cause of MS is not known, most circumstantial evidence has suggested that it is an autoimmune disorder wherein the immune system's defense mechanisms mistakenly destroy the myelin. Various drugs that modulate the immune system have been tested in multiple sclerosis and some of the most successful are interferon-beta and GA, which reduce the rate of relapse by about one third.
"Although IFN-beta and GA represent breakthroughs in the treatment of MS, neither compound is a cure for MS," Huang pointed out. "In fact, many patients with MS do not respond to treatment with either GA or IFN-beta."
Huang and her colleagues in a research group led by Hans Link, M.D., set out to probe how the drugs affected the immune system in the hope that they could be induced to do more. To that end, they examined how the two drugs act on dendritic cells, key players in orchestrating attacks by the immune system.
Their first accomplishment was to develop a method for studying immature dendritic cells taken from the blood of MS patients. This system allows them to expose the cells to different drugs and observe how the drugs affect their maturation.
The researchers found that both IFN-beta and GA increased the number of dendritic cells exhibiting a cell-surface marker called CD86 that stimulates cell responses believed to be beneficial in MS. In addition, both drugs lower the dendritic cells' production of interleukin-12, a molecule that directs other immune system cells to destroy invaders such as bacteria and possibly also the body's own myelin in MS.
IFN-beta also increased the number of dendritic cells producing the beneficial molecule interleukin-10, which helps shut down immune responses, such as the ones that may be harming myelin in MS.
However, because the two drugs exert their effects on different subsets of the dendritic cell population, the researchers suggest that combining IFN-beta and GA may provide better protection against MS.
An additional benefit of their work, the authors said, is that their system can be used by other scientists to study other potentially effective drugs on isolated dendritic cells.
Embargoed until 9:00 AM ET, Monday, October 1, 2001
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© 1995-2001 Newswise