Cancer Cells Use Regulatory T Cells to Activate Antitumor Immunosuppression

Cancer cells have evolved numerous ways to evade our immune system. An example of one of these ways is when a cancer cell generates a “don’t eat me” MHC1 signal on its cell surface to trick immune cells into thinking they are normal healthy cells. Recently, researchers from the University of Michigan School of Medicine have identified a novel way in which cancer cells fight back against our immune cells, specifically through T regulatory cells (Treg). Treg’s are responsible for sending signals to other immune cells to halt an immune response when an invading threat has been neutralized. However, during the development of any form of cancer, TReg’s would normally want to remain inactive in order to ensure that the cancer is constantly attacked by the immune system. In order to suppress the immune system from attacking cancerous tissue, cancer cells have evolved yet another way of tricking our immune systems by over stimulating the TReg signal. The general mechanism that the authors have identified is that when a TReg is attracted to a tumor microenvironment it will be met by free reactive oxygen species (ROS’s). TReg’s are unable to combat against ROS’s because they have weak NRF2-associated antioxidant systems, ensuring that when faced with ROS in the tumor microenvironment, the TReg’s will end up going through apoptosis. When a Treg goes through apoptosis it will convert all available ATP to adenosine through a CD39/73 dependent mechanism. This significant increase in available adenosine will lead to the induction of the A2A antitumor immunosuppression pathway, or in other words, a large scale signaling cascade informing all antitumor immune cells to stop fighting. It is through this mechanism that tumor’s are able to evade many kinds of immunotherapy, making researchers nervous about the future of using our on immune systems to treat cancer.

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