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Our immune system is an incredible machine composed of tiny soldiers (also known as immune cells) that work day and night to keep us healthy. Specialized cells, called T cells, play a crucial role in this process. Their incredibly elaborate machinery provides us with many layers of protection to fight any possible pathogens (“germs” that cause diseases) and cancerous cells they might encounter.
On a “regular” day, T cells remain in a “chill” state. Still, as soon as they recognize any danger and receive signals from other immune cells that something terrible is happening inside us, our T cells get activated and ready to fight! (If you want to know more about the way T cells fight, check out this post)
Yes, we want our T cells to fight, but we also don’t like this fight to last forever. As we talked about before, too much “fight” can cause real trouble and might even lead T cells to destroy our healthy cells, which is never a good sign. So, although “turning on” a killer cell is very important to fight infections, “turning off” these cells is just as important. Remember, we need a system that kills only what it needs to kill.
As with everything in immunology, there is not a single way or mechanism that tells our T cells to “calm down.” But today, I decided to talk to you about one component of this process that has been in my mind for a long time. Get ready to hear how PD-1 helps our T cells “hit the brakes!”

Pseudo-colored scanning electron micrograph of an oral squamous cancer cell (white) being attacked by two cytotoxic T cells (red), part of a natural immune response. Credit: Rita Elena Serda, Duncan Comprehensive Cancer Center at Baylor College of Medicine, National Cancer Institute, National Institutes of Health
PD-1 is part of a group of proteins that helps promote balance during an immune response. Together, these are known as immune checkpoints. These “break” proteins help decrease the function of our T cell soldiers, which is good as we don’t want our great fighters killing when there is nothing to kill.
Fascinating, right?! This incredible discovery did not go unnoticed. The 2018 Nobel Prize in Physiology or Medicine was awarded to Tasuku Honjo and James Allison for their discoveries in cancer immunology. Both professors discovered important molecules (PD-1 and CTLA-4) that act as T-cell breaks.
Ok, I get it, Stefanie. We get infected, our fighters will be activated and battle the intruder, and when they are done, we want them to “chill” so they don’t cause any unwanted damage. This is perfect, and nothing can go wrong, right?! Right?!
Well… not so fast. Sadly, cancer cells have evolved to use this T cell “break” mechanism to their advantage.
The “main goal” of cancer is to grow without having to deal with our immune system killing them. So, they express a molecule which will bind to the “break” protein (PD-1) expressed by T cells, telling our fighters to hit the breaks. Can you see the problem?
As our immune fighters decrease their function and return to a “chill” state, cancer cells can successfully “hide” from our immune system, allowing them to grow undisturbed.
Well, this is not good news. Please tell us that there is a way out!
Yes, there is a way out. Cleverly, scientists have designed molecules that can stop cancer cells from triggering the “breaks” on T cells. These are known as immune checkpoint inhibitors, and a few of these are already approved by the FDA (Food and Drug Administration) to treat patients with specific types of cancer. These molecules allow our immune soldiers to continue fighting their battle as they eliminate all cancer cells!
The cool thing about immune checkpoint inhibitors is that they don’t actually kill the cancer; these cells help our immune system do its job better. So, in the end, we can get all the credit for the fight!
PD-1 is also crucial in many other aspects of our immune system, but I will keep these other cool stories for another time. As for now, remember to keep asking questions and seeking answers!
From your immunologist – in training,
Stefanie Valbon, MSc, PhD candidate