Identifying regulators of PD-L1 to restore antitumor immunity
Tessa Simone | Green Lab | American Cancer Society Postdoctoral Fellowship
The immune system should recognize cancer as foreign in the same way is does viruses and bacteria. One way in which it goes wrong is the expression of a protein PD-L1 on the surface of tumor cells that acts as a stop sign to immune cells when it binds to another protein, PD-1, on the surface of immune cells. Recently, the Food and Drug Association has approved several drugs that inhibit PD-L1 and PD-1 that allows for immune cells to attack tumors for the treatment of several cancers.
These drugs have been widely successful in fighting cancers such as triple-negative breast cancer, melanoma and small cell lung cancer that don’t respond to traditional chemo-therapeutics. However, the drugs have one major unwanted side effect: autoimmunity.
The drugs are not intended for long-term use because they ramp up the immune system too well. When this happens, patients develop autoimmunity and the immune system attacks normal, healthy tissue.
We are working to identify the genes that cause PD-L1 to be expressed on cancer. If successful, they could potentially find drugs to inhibit these genes, and thus allow the immune system to attack tumors but spare normal tissue.
