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A DRUG designed thirty years ago to treat multiple sclerosis might suppress a
whole range of autoimmune diseases. It produces a shift in the immune system
that counteracts the way the body turns on itself, say researchers in the
US.

The body can mount two distinct types of immune response: Th1 or Th2. The two
are antagonistic鈥攕ignals that stimulate one inhibit the other and vice
versa. In multiple sclerosis, an inflammatory, Th1-type response destroys
proteins in the myelin sheath that covers nerves.

In 1967, researchers in Israel synthesised a drug made from amino acids found
in myelin basic protein. The drug, glatiramer acetate (GA), seemed to protect
the nerves of animals with MS-like diseases, presumably by attracting immune
system cells that would otherwise attack myelin. Patients given the drug also
had fewer relapses.

But now David Hafler at Harvard Medical School and his team have evidence
that the drug alters the immune system in a more general way. They analysed
T-cell lines from MS patients before and after a long course of GA treatment,
and then looked at how these cells responded to antigens such as myelin basic
protein, GA itself, and other proteins and peptides associated with autoimmune
disease.

After treatment with GA, T cells are more likely to cross-react with many
different peptides. Crucially, they also released Th2 cytokines: signals that
should elicit a Th2 response and counteract the Th1 response to the peptides
involved in MS.

鈥淚t was previously thought it worked by looking like the myelin protein,鈥�
Hafler says. But it 鈥渒ind of looks like everything鈥�, because it is a random
arrangement of four amino acids created before scientists knew precisely how to
generate a desired protein. Because GA stimulates a shift away from the damaging
Th1 response, Hafler believes that it could be useful for treating autoimmune
diseases caused by other antigens. Hafler points out that Igal Gery at the
National Institutes of Health near Washington DC recently found that the drug
protects mice against an autoimmune eye disease called uveoretinitis.

Roland Martin, of the National Institute of Neurological Disorders and Stroke
near Washington DC, has completed a similar but unpublished study of how GA
affects T cells. He says that it would be difficult to prove that the shift to
Th2 is truly the mechanism behind GA鈥檚 effectiveness against multiple sclerosis.
But he agrees that the theory makes sense.