Relapses Prevented In Mouse Model Of Multiple Sclerosis: Research Aimed At,,Treating Relapses I...( ase the number of Th1 cells -- and allo...)

ase the number of Th1 cells -- and allow Th2 cells to do their job -- demyelination could be suppressed. To do that, the researchers neutralized interleukin-12 with an antibody, which in turn suppressed the production of Th1 cells. Therefore, with less Th1 cells, the remaining Th2 cells were free to fight the inflammation caused by the Th1 cells.

In past experiments, researchers gave treatments to animals before disease symptoms were first seen, then waited to see if the EAE disorder would progress. Instead, Rostami's team waited until the mice had their first relapse before administering the experimental treatment. This design more accurately reflects the situation in humans, in which patients are given a treatment after the onset of a relapse.

"Those mice that received the antibody to interleukin-12 didn't relapse," notes Rostami. The same results hold true for superantigen-induced relapses, a model that is similar to human MS relapses triggered by viral or bacterial infections.

Drugs used to treat MS relapses such as interferons and Copaxone only decrease the number of relapses by one-third, notes Rostami, "so, we are always looking for better therapies." The next step is to produce the human form of the anti-interleukin-12 antibody and administer it to MS patients at the start of a relapse.

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Contact: Karen Young Kreeger
kreeger@mail.med.upenn.edu
215-614-0290
University of Pennsylvania School of Medicine
28-Oct-1998

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