
A team from the University of Cambridge and the University of Oregon Health and Science has discovered a new mechanism by which cancer cells evade immune pursuit, which may improve the problem of poor response to immunotherapy.
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Scientists have discovered that tumors can release natural substances that make immune cells lose their ability to attack, revealing a new mechanism for cancer cells to evade immune pursuit.
T cells are important players in the human immune system responsible for identifying and attacking abnormal cells. Latest research has found that cancer cells may interfere with the process of T cells initiating attack by releasing PRDX1 protein; schematic diagram.
The human immune system originally identifies and attacks cancer cells, but scientists have discovered that tumors can actually release a natural substance that makes immune cells lose their ability to attack and gain space for themselves to survive. This study reveals a new mechanism by which cancer cells evade immune pursuit and provides new research directions for improving the poor response of some cancer patients to immunotherapy.
The science news website "ScienceDaily" reported that this research was conducted by teams from the University of Cambridge in the UK and the University of Oregon Health and Science in the United States, and the results were published in the journal "Science". Research has found that cancer cells release a natural antioxidant protein called PRDX1 to remove specific substances in the surrounding environment, making it difficult for immune cells to launch an attack.
The key here is reactive oxygen species. Reactive oxygen species are often thought to harm cells, but T cells in the immune system also need an appropriate amount of reactive oxygen species to activate their function of attacking cancer cells. Studies have found that when tumors release PRDX1, these reactive oxygen species are consumed, causing T cells to lose the signals needed to initiate an attack.
The research team used gene editing technology to prevent mouse cancer cells from producing PRDX1. Experiments have found that after losing this protein, immune cell activity increases and tumor growth is also inhibited.
The researchers then examined human cancer cells and tumor data, and found evidence supporting this mechanism in the genetic data of thousands of tumors, as well as tissue fluid obtained from patients after surgical removal of tumors.
The research team further tested the impact of blocking PRDX1 on immunotherapy. In experimental models, some tumors that originally responded poorly to immunotherapy began to respond to treatment after destroying this defense mechanism.
The researchers said that studies have found that cancer cells use this method to shut down the immune system. After blocking the relevant mechanisms, some tumors that were originally unresponsive to immunotherapy began to respond to treatment.
The discovery also led researchers to re-examine the role of antioxidants. Although reactive oxygen species may damage cells, they are also an important signal for immune cells to initiate attack. Researchers believe that in the future, they may explore the use of pro-oxidant substances to help T cells restore their ability to attack tumors.
However, this research is still in the preclinical stage. Although researchers have found relevant mechanisms in human tumor samples, whether blocking PRDX1 can be used in cancer treatment, as well as its safety and effectiveness, still requires further study.

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