With the power to turn themselves into any other cell in the body, stem cells have a future as a key treatment for a range of diseases and injuries. The problem is, they lack some of the self-defense mechanisms that other cells have, leaving them open to attack from viruses and other threats. Now, researchers from the University of Edinburgh may have found a way to switch this mechanism back on, making stem cell treatments more effective.
When cells in the bodies of humans and other animals detect an invading virus, their immune system kicks in with a type I Interferon (IFN) response. But embryonic stem cells can't do that on their own. In the body they appear to be protected through some other unknown means, but in the lab or when used as a medicine, they're vulnerable to infection.
So the researchers on the new study examined stem cells from mouse embryos, trying to learn more about how stem cells resist viruses. They discovered a protein called the mitochondrial antiviral signalling (MAVS) protein that controls the IFN immune response in stem cells. MAVS usually seems to be switched off in embryonic stem cells, but the researchers also found a molecule known as miR-673, that in turn controls MAVS.
To test how these parts work together, the team cultured embryonic stem cells, and introduced viruses to two batches – a control, and one that had no miR-673. Sure enough, they found that stem cells without the molecule were far better at fighting off the virus than those with it, leading the researchers to conclude that miR-673 suppresses the immune response of cells.
So why would the body normally switch off this defensive system for stem cells? The team says that it might disrupt the development of embryonic stem cells, so the immune system defends them in some other way, further upstream, that we haven't discovered just yet.
While this is just a mouse study at the moment, the researchers are confident the same mechanism is at work in humans too. If so, identifying this molecule is an important step for stem cells as a medical treatment.
"Unveiling how this crucial antiviral mechanism is switched off, and methods to switch this back on in a controlled manner, could make stem cell therapies much more efficient," says Jeroen Witteveldt, co-author of the study.
The research was published in the journal eLife.
Source: University of Edinburgh
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