The body consists mainly of two types of immune cells. Innate immune cells are the first line of defense, targeting invaders at the first sign of an infection or inflammation. Adaptive immune cells, like T-cells, are more selective, attacking specific antigens.
Cancer cells have many ways of avoiding both immune responses. Because cancer cells are the body's own mutated cells, the immune system does not always recognize them as foreign. Cancer cells also may overpower innate cells, becoming too strong to be killed, or they may send deceptive signals at certain "checkpoints" that tell adaptive T-cells they are not harmful.
Checkpoint inhibitors work by disrupting the cancer cells' signals, exposing them to the T-cells for attack.
How they work
Certain protein receptors located on the surface of T-cells help differentiate healthy cells from cancer cells. Current checkpoint inhibitor drugs target the PD-1 and CTLA-4 receptors.
The PD-1 receptor seeks out the PD-L1 protein on other cells to determine if those cells are healthy. Cancer cells are able to disguise themselves as healthy cells by sending a signal to PD-1 using the protein PD-L1. Pembrolizumab (Keytruda®), nivolumab (Opdivo®) and atezolizumab (Tenectriq®) target the PD-1 receptor and disrupt the signal from PD-L1, exposing the cancer cell for attack.
Like PD-1, the CTLA-4 receptor helps the immune system target bad cells. CTLA-4 does not need to link with a specific protein to regulate an immune response. Ipilimumab (Yervoy®) rewires the CTLA-4 receptor to stimulate an immune system attack.
The U.S. Food and Drug Administration has approved specific checkpoint inhibitors to treat melanoma, Hodgkin lymphoma, bladder, kidney and/or lung cancer. Checkpoint inhibitors may be used in combination or in conjunction with other cancer treatments, such as chemotherapy and surgery.
Learn more about the treatment of melanoma.