![]() “We were a bit disappointed and thought we had hit a dead end because it looked like removing NRP1 did not impact anti-tumor immunity,” said Liu. When they grafted tumor cells to this mouse model, they expected that the tumors would not grow or grow more slowly when compared to normal animals, as they had seen when blocking other checkpoint proteins. Liu and her colleagues created a genetically modified mouse that had NRP1 removed specifically from the surface of only killer T cells. “We thought it might function like any other immune checkpoint molecule and that blocking it would prevent tumors from growing.” Chang “Gracie” Liu, Ph.D., a postdoctoral researcher in Vignali’s lab and first author of the publication. “We knew NRP1 was present on the surface of other T cells, but we wondered whether it somehow altered the function of the killer T cells,” said Dr. Vignali and his colleagues discovered that a protein called Neuropilin-1 (NRP1) plays an important role in suppressing immune responses to cancer. “Our findings point to an important new biological anti-tumor mechanism that we can exploit to provide durable, long-term immune response against tumors.” Vignali, Ph.D., who holds the Frank Dixon Chair in Cancer Immunology at Pitt’s School of Medicine and is the co-leader of the Cancer Immunology and Immunotherapy program at the UPMC Hillman Cancer Center. “There is still much work to be done to improve cancer immunotherapy because only a small group of people benefit, and even among those, we see many tumors relapsing,” said Dr. However, only about a third of patients respond to these drugs. They work by blocking checkpoint inhibitor proteins like PD1, removing the brakes from cancer-killing T cells in the immune system. Immunotherapy drugs that harness the body’s own immune system to fight cancer have revolutionized the treatment of many cancers. The research was published this week in Nature Immunology.
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