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.
Mar 9 2024NYU Langone Health 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.
Among the most important checkpoints is a protein called programmed cell death receptor 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.
Study results showed that PD-1 forms a dimer through interactions of its transmembrane segment. Researchers say this finding is in sharp contrast to other immune receptors, which typically form dimers through the segment of the receptor that is outside the cell. Elliot Philips, MD, PhD, Study Lead Investigator and Physician-Scientist, NYU Grossman School of Medicine
Related Stories"Our goal is to use our new knowledge of the functioning of PD-1 to determine if weakening its dimerization, or pairing, helps make anticancer immunotherapies more effective, and just as importantly, to see if strengthening its dimerization helps in the design of agonist drugs that quiet overactive T cells, tamping down the inflammation seen in autoimmune diseases," said study co-senior investigator and structural biologist Xiang-Peng Kong, PhD.
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