Claudia Wallis in Scientific American:
In health, as with so many things, our greatest strength can be our greatest weakness. Take our astonishingly sophisticated response to injury and infection. Our bodies unleash armies of cellular troops to slaughter invaders and clear out traitors. Their movements are marshaled by signaling chemicals, such as the interleukins, which tell cells where and when to fight and when to stand down. We experience this as the swelling, redness and soreness of inflammation—an essential part of healing. But when the wars fail to wind down, when inflammation becomes chronic or systemic, there's hell to pay. I'm looking at you, arthritis, colitis and bursitis, and at you, diabetes, colon cancer, Alzheimer's and cardiovascular disease.
Cardiovascular disease is the world's biggest killer, and we've known for 20 years that inflammation (along with too much cholesterol) ignites the buildup of plaque in our arteries. Still, no one knew if runaway inflammation could actually pull the trigger on heart attacks and strokes—until this summer. Results from a large, well-designed trial showed that certain high-risk patients suffered fewer of these “events” (as doctors so mildly call them) when given a drug that precisely targets inflammation (aiming at interleukin 1). It was sweet vindication for cardiologist and principal investigator Paul Ridker of Harvard University, director of the Center for Cardiovascular Disease Prevention at Brigham and Women's Hospital, who had long contended that inflammation was as vital a target as cholesterol.