A recent study conducted by researchers from the Perlmutter Cancer Center at NYU Langone Health and the University of Oxford reveals a major breakthrough in the fight against cancer and autoimmune diseases. The key to this breakthrough lies in understanding the role of the receptor on the surface of immune cells, PD-1.
The new research shows that the immune receptor PD-1 functions better as dimers, contrary to previous beliefs. This discovery is crucial for improving cancer immunotherapies and treating autoimmune diseases by targeting the dimerization of PD-1.
The study, published in the journal
Science Immunology, sheds new light on the immune system, particularly its ability to distinguish cancer cells from normal cells through "checkpoints." PD-1, one of these checkpoints, plays a crucial role in protecting normal cells against immune attacks. Cancers, however, manage to exploit this mechanism to become "invisible" to the immune system.
Researchers have discovered that PD-1 functions by forming dimers, a paired configuration, through interactions within its transmembrane segment. This discovery challenges the preconceived notion that PD-1 operated solo. By manipulating the formation of these dimers, it could be possible to enhance the effectiveness of cancer treatments and design drugs for autoimmune diseases by modulating the activity of T cells.
The study highlights the potential of agonists, drugs that stimulate PD-1, in treating autoimmune diseases such as rheumatoid arthritis, lupus, and type 1 diabetes. These diseases result from an overactive immune response causing inflammation and damage to tissues. By activating PD-1, these strategies aim to block this hyperactive immune response.
Researchers now aim to use this knowledge about how PD-1 functions to optimize anticancer immunotherapies and design new treatments for autoimmune diseases. Their discovery paves the way for more effective "rationally designed" therapies, by manipulating the dimerization of PD-1 to regulate the function of T cells.