Scientists from The Scripps Research Institute and the University of California discover possible master switch for programming cancer immunotherapy
Cancer immunotherapy is a treatment in which immune system is used for treating cancer patients. Mostly cancer cell has a molecule on their surface known as tumour associated antigen(TAA) which can be recognized by the immune system.
During infection or tumour growth, diseased cells are killed by the specialized WBC called CD8+T cells which actively divide within the spleen and lymph nodes then migrate to other areas where germs and cancer cells are present.
For developing cancer-fighting immunotherapy strategies, it is important to find that how T cells leave their site and go beyond the lymphoid system and migrate to the specific tissue or in a solid tumour.
In a recent article published in journal Nature, researchers from The Scripps Research Institute and the University of California, San Diego, discovered a protein which drives the T cells to migrate to tumour and infection sites.
The author Matthew Pipkin, Ph.D., associate professor in the Department of Immunology and Microbiology on the Florida campus of The Scripps Research Institute, says that the reason behind the accumulation of T cells in a solid tumour is the gene Runx3 present in the chromosome inside the killer T cell which controls it and helps in employing T cell in cancer immunotherapy.
Two main approaches for cancer immunotherapy were checkpoint inhibitor and adoptive cell transfer. Former releases killer T cell stimulating them to accumulate in tumour more aggressively while the later strategy deals with engineering the patient’s own immune cells in the lab so that they can recognize and kills specific cancer in the patient body. After engineering, they are reintroduced in a patient body.
In blood cancer associated with a lymphoid system, the adaptive strategy worked very well but the activity of T cell in tumour is less effective. Mechanism of gene signaling T cell function beyond the general circulation was not understood.
In the light of this, Pipkin team collaborated with other researcher and they compared CD8+T cells gene expression in non-lymphoid tissue with those found in general circulation and applied RNA interference strategy which can help to investigate the actual role of thousands of factors altogether.
They found out a distinct pattern during the study. The RNA interference screening revealed that Runx3 is the essential regulator for T cell to reside in lymphoid tissue could involve a specific gene program that is found in natural tissue-resident and tumour infiltrating CD8+ T cells.
According to the researcher, if the Runx3 activity is enhanced, tumour growth is delayed compared to control group and this gene also influence the ability of cancer-specific t killer cell to reside in a solid tumour which unseals new opportunities in cancer immunotherapy.