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    Home > Active Ingredient News > Immunology News > Nat E. Ni Yu's new team reveals a new mechanism for tumor immunity.

    Nat E. Ni Yu's new team reveals a new mechanism for tumor immunity.

    • Last Update: 2020-07-22
    • Source: Internet
    • Author: User
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    The development and metastasis of malignant tumor is the result of the game between malignant tumor and immune system.tumor cells can escape the attack of immune cells by inducing T lymphocyte depletion.in recent years, PD-1 antibody therapy has been widely used in tumor immunotherapy by blocking the depletion of T lymphocyte function and restoring the activity of T cells.however, only 20% of patients respond to PD-1 antibody therapy.therefore, it is of great significance to explore the mechanism of tumor affecting the function of T lymphocytes, and to clarify the reason why T lymphocytes function exhaustion in tumor microenvironment, which is of great significance to identify new tumor immune targets and develop new effective tumor treatment strategies.on January 13, 2020, Professor Yin Yuxin from the Institute of Systems Biomedicine, Peking University published the title of "the phosphotase PAC1 acts as a T cell suppressor and attenuates host antitumor" in the journal Nature Immunology As a negative regulator of immune system, phosphatase PAC1 can specifically inhibit T lymphocyte defense function and promote tumor immune escape.through systematic analysis of inflammatory factors and metabolites in tumor microenvironment, Yin Yuxin's team found that ROS produced by tumor can maintain high expression of PAC1 gene in peripheral infiltrating T lymphocytes.further studies have shown that ROS promotes the transcription and expression of PAC1 by activating transcription factor EGR1.in 2003, Professor Yin Yuxin reported for the first time the research on the role of PAC1 in tumorigenesis and development in nature, and proposed that PAC1, as a phosphatase specifically expressed in the immune system, may participate in the formation and remodeling of tumor microenvironment [1].in 2015, Professor Yin Yuxin's research team published a research paper in Nature Immunology, revealing that PAC1 (dusp2) inhibits Th17 cell differentiation by regulating the activity of transcription factor STAT3, thus inhibiting the occurrence and development of autoimmune diseases [2].in view of PAC1's strong immunomodulatory ability, the research group then explored whether PAC1 could become a new tumor immunotherapy target.this study found that PAC1 was highly expressed in depleted T lymphocytes.the higher the expression of PAC1, the worse the prognosis.further studies showed that PAC1 inhibited the killing function of CD8 + T cells to tumor cells, induced the formation of depleted T lymphocytes, and promoted the immune escape and metastasis of tumor.in terms of mechanism, PAC1 can extensively influence the expression and function of downstream effector genes by recruiting nucleosome remodeling and deacetylation (NuRD) complex to remodel the chromatin openness of T cells.ros-egr1-pac1 signaling pathway is involved in inducing T lymphocyte function depletion. In conclusion, PAC1, as an important suppressor of T lymphocyte function, can weaken host immune surveillance function and promote tumor immune escape.inhibition of PAC1 pathway can activate the defense function of T lymphocytes. This study provides a potential new drug target for tumor immunotherapy. associate researcher Lu Dan and postdoctoral Liu Liang of School of basic medicine of Peking University are the co first authors of this paper, and Professor Yin Yuxin of Institute of Systems Biomedicine of Peking University is the corresponding author. < br / < br / < br / < br / < br / original link: Reference: 1.yin, y, *, Liu, y.x., Jin, Y.J., hall, E.J., and Barrett, J.C. (2003) (2003). PAC1 phosphate is a transcription target of p53 in signaling apoptotsis and growth suppression. Nature 422: nature 422: 527-531.2.lu, D., Liu, L., Ji, X., Gao, Y., Chen, X., Li, X., Li, X., Li, Y., Li, Li, Li, Li, Li, Li, Li, Li, Li, Li, Li, Li, Li, Li, Li, Li, Li, Li, Li, Li, Li, Li, Li, Li, Li, Li, Li, Li, Li Jin, Y., Zhang, y, McNutt, M.A., and Yin, Y. * (2015). The phosphotase dusp2 controls the activity of the transcription activator STAT3 and regulations Th17 differentiation. NAT Immunol., 16, 1263-1273
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