When you’re fighting flu or any other infection, your body mobilizes battalions of cells to defend against the invading viruses or bacteria. But once the invaders have been defeated and you’ve recovered from aches, fever, headaches, and a sore throat, your body has to get rid of the now-unneeded fighting cells. If left alone, they can attack healthy tissues.
One way to muster them out is signaling them to commit suicide. Sounds cruel, but it’s a natural protective process called “apoptosis.” It is the same strategy that the human immune system uses to get rid of tumor cells.
But the old soldiers don’t go peacefully. Researchers at the Harvard Medical School have discovered that, on their way out, they grab onto and remove chemicals that would otherwise promote inflammation. Said another way, they keep the body from attacking itself.
“Failure to clear the apoptotic white blood cells can result in a lupus-like syndrome and accelerated atherosclerosis,” notes Charles Serhan, Simon Gelman Professor of Anaesthesia and leader of the research. In lupus, the immune system attacks the body’s connective tissues; atherosclerosis leads to clogged or narrowed blood vessels.
Serhan, working with Amiram Ariel, a research fellow, and other collaborators at Brigham and Women’s Hospital, Boston University, and Massachusetts General Hospital, found that the dying cells carry a protein on their surface that permits them to bind to and remove harmful chemical leftovers. The team demonstrated this previously unknown function in rabbits, mice, and cells from humans.
The suicide process increases the amount of scavenger protein that is carried by dying soldier cells. The scavengers in turn are engulfed and cleared out of the body by bigger cells known as macrophages.