Do we need a psychiatrist for our immune system?
Imagine if you lost the ability to see in one eye or were unable to feel a part of your arm. Either of these things, among others, could happen to you at any time if you had multiple sclerosis (MS). MS is an autoimmune disorder that sporadically damages myelin, the part of brain cells that allows them to respond quickly. When the myelin is gone, signals between your brain and the rest of your body are sent much, much slower. The damaged brain cells are fixed by the body over time and the symptoms disappear over time. But more damage eventually occurs and the symptoms come back, each time different than the last.
But what causes MS in the first place?
A group of scientists from Boston recently found that infection with Epstein-Barr virus (EBV) increases one’s chance of developing MS. Our bodies are filled with and surrounded by approximately 380 trillion viruses – 12 times the number of cells that make up a person. Parts of these viruses could be similar to our cells. And when our immune system learns to fight the viruses, it may inadvertently attack our own cells too. This is presumably what is happening in MS – the virus and the myelin are similar in some way and our immune system is tricked into attacking the myelin on brain cells, believing it is actually EBV.
If we could know who has been infected with EBV, could we monitor them more closely and prevent even the first attack of MS? More broadly, if we could know what viruses are living in us, could we determine which currently unexplained illnesses are caused by viruses? Researchers in Seattle think they can do just this by looking at immune cells.
Our immune system is our first line of defense against infections. While some immune cells act like fences, preventing germs from getting into cells, others act like snipers – eliminating the enemy once it has already made it past the fence. “T cells” are the snipers. When they see harmful viruses in our cells, they react – they make more copies of themselves and then attack the virus-infected cells. Once the threat has been neutralized, the some of the responding T cells become “memory” cells, lying in wait until the same virus comes in again. Just like a psychiatrist tries to identify the root of a person’s problem, we may soon be able to know what viruses we have been infected with by finding out which of our T cells have reacted to a threat.
T cells see viruses that are present in our cells with molecules on their surface called “receptors.” T cell receptors that recognize the same virus are like each other. And we are now increasingly able to detect similar patterns in T cell receptors and predict which virus a T cell is poised to fight. Researchers at the University of Washington and the Fred Hutchinson Cancer Research Center are perfecting a tool that can predict whether a T cell is seeing the virus that causes a deadly skin cancer, Merkel cell carcinoma.
Once refined, similar tools can be developed for other viruses until we can metaphorically ask a T cell what virus triggers it. And if we see many copies of the same T cell, we know that it was once activated and that we have previously come across the virus that it recognizes. With this knowledge, the possibilities for scientific progress are vast, and include identifying viral causes of currently unexplained illnesses and determining how well our immune system is fighting an infection or a virus-driven cancer.
Saumya Jani is a graduate student researcher in the University of Washington’s Department on Lab Medicine and Pathology. She is studying the immune response to an aggressive and often lethal skin cancer, Merkel cell carcinoma, in order to improve immune-based cancer treatments.