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summarize the key points of the article: A study reveals insights into how the immune cell surface receptor PD-1 works and how treatments restricting its action can be strengthened for better anticancer effects. By stimulating PD-1 instead of restricting it, overactive immune responses in autoimmune diseases can potentially be blocked. Checkpoint inhibitors targeting PD-1 can make tumors "visible" to the immune system, but ways to improve their effectiveness and scope are still being sought.
Insights into the workings of an immune cell surface receptor, called PD-1, reveal how treatments that restrict its action can potentially be strengthened to improve their anticancer effect, a new study shows. The same findings also support experimental treatment strategies for autoimmune diseases, in which the immune system attacks the body, because stimulating the action of PD-1, as opposed to restricting it, can potentially block an overactive immune response.
Led by researchers at NYU Langone Health’s Perlmutter Cancer Center and the University of Oxford, the study is publishing in the journal Science Immunology online March 8.
The study results revolve around the body’s immune system, which is primed to attack virally infected and cancerous cells while leaving normal cells alone. To spare normal cells from immune attack, the system uses “checkpoints,” sensors on the surface of immune cells, including T cells, which turn them off or dampen activation when they receive the right signal. The immune system recognizes tumors as abnormal, but cancer cells can hijack checkpoints to turn off immune responses.
Among the most important checkpoints is a protein called programmed cell death receptor 1 (PD-1), which is shut down by a relatively new drug class called checkpoint inhibitors to make tumors “visible” again to immune attack. Such drugs are at least somewhat effective in a third of patients with a variety of cancers, say the study authors, but the field is urgently seeking ways to improve their performance and scope.
At the same time, PD-1 signaling is