Abstract

Atherosclerosis is the most common cause of heart disease, but the condition is largely misunderstood. When the average person thinks of atherosclerosis, they imagine blood vessels narrowed by the buildup of thick, sticky fats, much like a clogged kitchen drain. In reality, that’s only half the story. The immune system also plays a part: in trying to heal the lesions, it reacts to plaques with inflammation, which further hardens and narrows blood vessels. This deeper understanding of how atherosclerosis arises offers new avenues for both treatment and prevention of heart disease, the leading cause of death worldwide. Filip Swirski, Research Scholar and Principal Investigator at Massachusetts General Hospital and Associate Professor of Radiology at Harvard Medical School, is a leader in studying the role of the immune system in cardiovascular disease. Trained as an immunologist at McMaster University, he is now applying his knowledge of innate immunity and inflammation to the study of atherosclerosis and, more recently, other diseases, as varied as sleep disorders, sepsis, Alzheimer, and colitis. Filip Swirski As a postdoctoral researcher, he began to explore the role of leukocytosis, and monocytosis in particular, in atherosclerosis. Monocytes are part of our innate immunity, the body’s ancient surveillance system that flags dangers, pathogens, and injuries. Swirski’s work demonstrated that these inflammatory cells are recruited to growing atherosclerotic lesions. He found that monocytes accumulate continuously as the lesions progress.1 His work was among the first in a growing field that has defined the essential role of monocytes and systemic inflammation in atherosclerosis. Monocytes usually mature into immune cells known as macrophages. These scavenger cells are responsible for devouring invaders and other dangers. But in the case of atherosclerosis, this protective mechanism backfires. Macrophages devour lipid plaques in the blood vessel wall, spurring inflammation, and narrowing the lumen. Swirski identified …

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