Magazine article Newsweek

When the Body Attacks Itself

Magazine article Newsweek

When the Body Attacks Itself

Article excerpt

Byline: Anne Underwood

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 seriously 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, director of the Immune Tolerance Network at 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 London posed that very question in the mid-1980s. Doctors scoffed. But three drugs for rheumatoid arthritis emerged from their research, and the same drugs are also proving useful for conditions like Crohn's disease and juvenile arthritis. This year Maini and Feldmann won the Lasker Award for clinical medical research. And some of their colleagues are talking Nobel Prize.

Drug companies are eager to expand this approach into therapies for other autoimmune diseases, which have been on the increase since the 1950s, but have few good treatments available today. Translating principle into practice will not be easy, however. 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 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. In a small clinical trial, they tested an anti-TNF antibody in 20 patients who had failed to respond to other treatments. Within hours, the recipients started feeling better. In six weeks, they were climbing stairs and even golfing. Today there are three TNF blockers on the market for rheumatoid arthritis--Remicade (which Maini and Feldmann used), Enbrel and Humira.

But not all patients with rheumatoid arthritis respond to these costly TNF blockers--nor does anti-TNF therapy hold the master key to all autoimmune diseases. "There may be some therapies that are broadly applicable across a wide range of disorders, and others that are particular to one disease," says Bluestone. …

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