To examine the source of this tissue buildup — called fibrosis — researchers at the Massachusetts Institute of Technology in Cambridge systematically removed different components of the immune system in mice. When cells called macrophages were removed, scar tissue did not form around implanted devices, according to the report.
Researchers then identified a signaling molecule that plays a role in stimulating macrophages to commence fibrosis. When they blocked the cell surface receptors for the molecule, it prevented the tissue growth, yet did not interfere with other critical functions the macrophages carry out in the body, according to the report.
“We show that you preserve many other important immune functions, including wound healing and phagocytosis, but you lose this fibrotic cascade,” lead author Joshua Doloff, a postdoctoral scholar at MIT’s Koch Institute for Integrative Cancer Research, told Science Daily “It’s generalizable to many different types of biomaterials, and hopefully will also be generalizable to many platforms for different purposes.”
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