Source: New Atlas
Date: December 11th, 2019
Author: Michael Irving

The immune system is already our best defense against cancer, but sometimes it needs help. After all, cancer has a knack for deceiving it and hiding from immune cells, giving itself time to grow and spread. Now, researchers at QIMR Berghofer Medical Research Institute in Australia have identified one way it does so, and found a method to counter it in mouse tests.

T and NK cells act like the foot soldiers of the immune system, searching the body for invading pathogens and attacking them. But their activity can be regulated by other immune cells, such as mucosal-associated invariant T cells (MAIT cells), telling them when to attack and when to stand down.

During the new study, the QIMR researchers discovered that if MAIT cells were switched on, they would prevent T and NK cells from attacking tumors. The tumors seem to have figured this out too – the team found that cancer cells actively turn on MAIT cells by displaying molecules called MR1 on their surfaces.

“The cancer is effectively creating its own defence mechanism to evade immune attack and survive,” says Michele Teng, senior researcher on the study. “The display of MR1 activates the MAIT cells, which in turn switch off cancer-fighting T and NK cells. While other regulatory cells of the immune system are known to stop T and NK cells from killing tumor cells, this is the first time it’s been shown that these regulatory MAIT cells can do this job.”

Understanding this mechanism could lead to new immunotherapy treatments. The team tested the idea in mice, by giving the animals antibodies that block MR1. Sure enough that prevented MAIT cells from switching on, increased the attack power of T and NK cells and ultimately slowed the growth and spread of the cancer.

“This work demonstrates that antibodies that block MR1 could in future be an effective new immunotherapy,” says Teng. “It probably won’t work on every cancer, but it looks like it could be effective in treating cancers that can display the MR1 molecule. It also means this display of MR1 could be used to screen which patients would respond to this immunotherapy.”

The team says that the next step is to try to replicate the results in humans, starting by determining which human tumor types use MR1.


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