Researchers have found out that removing a key immune regulator called PTPN2 can accelerate anti-cancer immunity. The immune system needs to maintain a balance between cancer infections and restraining the activity at the same time, which can harm healthy tissues and body organs. The scientists have demonstrated the trial on the immune system of mice recently. They found out that deleting the PTPN2 gene stimulates the production and health of T Killer cells. T Killer cells are part of the body’s adaptive immune system. They are critical in warding off virus and bacteria. There are immense similarities between the immune system of mice and humans. These findings can be touted as a milestone achievement in the cancer research field.
This technique targets a particular immune regulator to boost the body’s anti-tumor response. It can be proved as a catalyst in cancer treatments. However, further experiments need to be carried out in animal and human clinical trials. Scientists have developed class immunotherapy known as ‘checkpoint blockade inhibitors in the mid-2000s. These therapies are used to treat various types of cancers such as colorectal cancer, Melanoma, and non-small cell lung cancer. Investigators have combined PD-1 checkpoint blockade with the deletion of the Immune regulator to come up with results that are more specific. It has eliminated treatment-resistant Melanoma in one-fourth of the mice. Scientists feel that the deletion of PTPN2 genes can help immune cells overcome cancer dysfunction. This phenomenon is called as ‘T cell Exhaustion’.
PTPN2 decreases the immunity by reducing the frequency of progenitor T cells maturing into T killer cells. This process is known as ‘Cytotoxic T cells’. Scientists found out that deleting immune regulator has induced the robust production of T killer cells in the presence of viral infection. T cells of mice having no PTPN2 were better at eradicating tumors said the first author of the study, Martin LaFleur. Researchers have also said that developing some compounds, which can block the activity of PTPN2, can be a second approach to this phenomenon.