A new mechanism of tumor immune escape has been discovered

and metastasis of malignant tumors is the result of their game with the body's immune system. Tumor cells induce T lymphocytes to run out of function to evade the identification and attack of the body's immune system, a process called tumor immune escape. Recently, scientists discovered a new mechanism of tumor immune escape, the study was published on January 14th in Nature -Immunology.
After analyzing inflammatory factors and metabolites in the tumor microenvironic environment, the team found that the reactive oxygen freelancer in the tumor microenviron environment activates the transcription factor EGR1, resulting in high levels of expression of phosphatase PAC1 in CD8-T lymphocytes (CD8-T).
CD8-T is a T lymphocyte with lethal function, which play a central role in tumor immunity, and how to activate such cells is the focus of research in this field. As a specific inhibitor of T lymphocytes, PAC1 not only inhibits CD8-T amplification, but also inhibits its cytokine secretion, reducing its ability to kill tumor cells.
the team found that after PAC1 was missing, cd8-T increased lethality, promoted an anti-tumor immune response, and inhibited tumor development and metastasis. Therefore, inhibiting the PAC1 signaling path, can activate the defense function of T lymphocytes.
this study provides a potential new drug target for tumor immunotherapy. "PAC1 is a more upstream negative immune regulatory factor than the now well-known PD-1, which reduces the expression of multiple inhibitory receptors, including PD-1. If the targeted PAC1 intervention, can better enhance the CD8-T-mediated anti-tumor immune effect. Lu Dan, co-first author of the paper and an associate researcher at Peking University's School of Basic Medicine, told China Science Daily. (Source: Ren Fangyan, China Science Journal)
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