Breach! Scientists have found a key switch protein that can effectively program cancer immunotherapy!

During the period of infection or tumor growth, a special type of white blood cells called CD8 + T cells will rapidly proliferate in the spleen and lymph nodes, and acquire the ability to kill disease cells; then some killer T cells will migrate to the affected area of the body to kill bacteria or cancer cells So how do these killer T cells learn to accumulate in special tissue parts (such as skin, advocacy, solid tumor parts) after leaving the "nest"? For a long time, researchers have failed to clarify which factors can promote the function of T cells beyond the lymphatic system and play a role in infection or cancer sites, which may be crucial for the effective development of new anti-cancer immunotherapy Recently, in a research report published in the international journal Nature, researchers from Scripps Research Institute and the University of California found that a special protein called RUNX3 can "program" killer T cells to help them build "shelter" in tumors and infection sites Dr Matthew Pipkin said that in killer T cells, RUNX3 protein can play a role in chromosomes to program genes in a special way, so as to help T cells accumulate in solid tumors At present, two main cancer immunotherapies are developed based on the employment of killer T cells Checkpoint inhibitors can block the release of killer T cells and promote their accumulation in malignant tumors At the same time, an alternative cell is called adoptive cell Transfer (ACT) is to inject the immune cells of the researchers after the engineering operation in the laboratory back into the patient's body to help the patient effectively recognize and destroy the cancer cells in the patient's body This adoptive cell transfer therapy performs well in many blood cancers associated with the lymphatic system, but does not seem to give T cells better activity in solid tumors At present, researchers have not fully elucidated how T cells use gene programming and signaling pathways to "live" in tissues outside the body's systemic circulation In order to find out the factors that can control T cell habitation, the researcher Pipkin and his colleagues, through a joint study, compared the gene expression in CD8 + T cells in non lymphoid tissues and the circulation of the body From the list of potential factors, the researchers used RNA interference screening technology to detect the real function of thousands of factors We found different patterns, and the screening results showed that RUNX3 was the most important regulator in the list of regulators that could help T cells to "settle" in non lymphoid tissues In addition, RUNX3 could also participate in special gene expression programs in natural tissues and tumor infiltrated CD8 + T cells The researchers then evaluated whether RUNX3 can directly regulate the leukocyte attack on solid tumors by studying the mouse model of melanoma The results showed that adoptive cell transfer of cancer-specific T cells overexpressing RUNX3 might slow down the growth of tumor and prolong the moderate survival period, while using the deletion RUNX3's therapeutic mouse models may be much worse than normal The researchers believe that if it can enhance the activity of RUNX3 in cells, the tumor size may be significantly reduced, and the survival rate of mice is higher than that of the control group Now researchers know that regulating the activity of RUNX3 in T cells can affect the accumulation of T cells in solid tumors, so this may help researchers improve the current cancer immunotherapy Finally, the researchers said that in the future, we may be able to use RUNX3 to reprogram the adoptive transfer cells, so as to drive these cells to be fierce in solid tumors Of course, in the later stage, we will conduct more in-depth research based on the results of this paper, so as to provide new ideas and hopes for the development of new cancer immunotherapy.