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The immune system is a thing of beauty--subtle enough to distinguish dangerous invaders like viruses from benign interlopers such as food; clever enough to recognize when the body's supposedly friendly cells turn cancerous and should be eliminated. But the immune system can also go awry. When it begins mauling healthy tissues, the result can be any one of 80 autoimmune diseases such as lupus or rheumatoid arthritis. "It's the price we pay for having such a dynamic, finely balanced system," says immunobiologist Jeffrey Bluestone of the University of California, San Francisco.
Must we limit ourselves to treating the symptoms of these disorders, or could we modulate the immune system itself? Immunologist Marc Feldmann and rheumatologist Ravinder Maini of Imperial College in London posed that very question in the mid-1980s. Doctors scoffed. But three drugs for rheumatoid arthritis emerged from their research. And this year Maini and Feldmann won the Lasker Award for clinical medical research.
Drug companies are eager to expand this approach into therapies for other autoimmune diseases, which have been on the increase since the 1950s, but it won't be easy. The immune system is a vast network with a bewildering array of warriors--from antibody-making B cells to various kinds of T cells that can enhance antibody production, kill virus- infected cells, initiate inflammation and finally shut down an immune attack. B cells and T cells also make more than 100 types of helpers called cytokines that assist in orchestrating every aspect of the immune assault.
Maini and Feldmann in the 1980s zeroed in on one such cytokine called tumor necrosis factor (TNF). It derives its name from its ability to kill cancer cells, but in excess it also initiates the inflammation of rheumatoid arthritis. Today anti-TNF therapy is proving useful for a range of inflammatory conditions. But ...