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Medical devices implanted in the body for drug delivery, sensing, or tissue regeneration usually come under fire from the host's immune system. Defense cells work to isolate material they consider foreign to the body, building up a wall of dense scar tissue around the devices, which eventually become unable to perform their functions.

Researchers at MIT and Boston Children's Hospital have identified a signaling molecule that is key to this process of fibrosis, and they have shown that blocking the molecule prevents the scar tissue from forming. The findings could help scientists extend the lifespan of many types of implantable medical devices.

"This gives us a better understanding of the biology behind fibrosis and potentially a way to modulate that response to prevent the formation of scar tissue around implants," says Daniel Anderson, an associate professor in MIT's Department of Chemical Engineering, a member of MIT's Koch Institute for Integrative Cancer Research and Institute for Medical Engineering and Science, and an affiliate at Boston Children's Hospital.

Anderson's lab has been working for several years on an implantable device that could mimic the function of the pancreas, potentially offering a long-term treatment for diabetes patients. The device encapsulates insulin-producing islet cells within a material called alginate, a polysaccharide naturally found in algae. Alginate provokes a lesser immune response than human-made materials such as metal, but it still induces fibrosis.

To investigate how fibrosis happens, the MIT team systematically knocked out different components of the immune system in mice. They found that cells called macrophages are necessary for fibrosis to occur, and that when those cells are missing, scar tissue does not form around implanted devices.

The researchers then identified a signaling molecule that appears to help macrophage precursors, known as monocytes, differentiate into mature macrophages, which then initiate fibrosis. They also discovered that if they blocked the cell surface receptors for this molecule, known as CSF1, they could prevent implant-induced fibrosis from occurring.

Importantly, this interference did not stop macrophages from carrying out other critical functions.

The researchers showed that blocking CSF1 receptors prevented fibrosis not only with alginate but also ceramic and a plastic called polystyrene.

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