JDRF funded researchers at the leading Massachusetts Institute of Technology have identified the cause of tissue scarring that makes life challenging for people who use technological devices like insulin pumps and CGMs.
Why did the study take place?
The researchers were trying to understand how the immune system response causes fibrosis – tissue thickening and scarring – when reacting to implanted materials, including infusion sets and CGMs. Currently, anyone who uses insulin pumps and CGMs must regularly change the site on their body where they place the devices, as the fibrosis that results from the body’s natural immune response to the ‘foreign’ material can prevent the tech from working properly.
This response also affects devices that are implanted completely within the body, such as the encapsulation products currently being developed as a transformative treatment for type 1 diabetes. This is an ongoing challenge facing the development of encapsulation (a therapy in which beta cells are placed inside a physical device which can protect them from the immune response once implanted beneath the skin) as it is the immune response to the device itself that leads to fibrosis, which in turn can impair the work of the device and cause discomfort to wearers.
How did they investigate the tissue scarring?
The researchers studied implanted devices in mice, and found that a particular type of immune cell, macrophages, were the main cause of the scarring around the devices. Macrophages are important in a healthy immune system as they act like bin lorries, engulfing and eating damaged or foreign cells.
If we removed all macrophages, an individual’s wider health would be at risk. The team suspected, however, that there might be a specific protein that was responsible for directing the macrophages to the device. They found that if they blocked a protein called colony stimulating factor 1, they were able to stop tissue scarring around the device, but not stop the good work of the macrophages. Colony stimulating factor 1 tells immune cells to turn into macrophages when it encounters a device, and so by stopping this message before it reaches the cells, the team were able to prevent the tissues scarring.
With the knowledge to prevent the immune response that results in implantable devices becoming surrounded by thickened tissue and scarring, we may be able to improve the success of implantable devices. This finding could also help reduce scarring for wearers of existing devices, like insulin pumps and CGMs.
Originally written by Angela Wipperman, published at JDRF
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