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Protein IDed to Cut Implanted Device Immune Reactions

Macrophage cell

Macrophage cell, in blue, blocked from forming into scar tissue. (Felice Frankel, Mass. Institute of Technology)

20 March 2017. Researchers identified a protein playing a key role in promoting the scar tissue that forms from immune reactions to implanted medical devices. A team from Massachusetts Institute of Technology and Boston Children’s Hospital shows in tests with lab animals that blocking actions of this protein can prevent scar tissue from forming on materials often used with medical implants.

In an article appearing 20 March in the journal Nature Materials (paid subscription required), researchers from the MIT labs of chemical engineering professors Robert Langer and Daniel Anderson sought to better understand the process causing immune reactions to medical implants. Anderson’s lab in particular is developing an implanted device to perform the functions of the pancreas, monitoring glucose levels and pumping insulin, for people with type 1 diabetes, an autoimmune condition affecting 5 to 10 percent of individuals with diabetes.

The team analyzed the general or innate immune functions as well as reactions of the immune system to specific foreign substances like those found in implanted devices. They traced the formation of scar tissue to a type of white blood cell in the immune system known as macrophages that are formed from precursor cells called monocytes. When tissue damage, infection, or foreign substances appear, monocytes transform into macrophages to become the first line of defense against these disruptions.

A key ingredient in the transformation of monocytes into macrophages is a protein called colony stimulating factor 1 receptor, or CSF1R. In tests with lab rodents and monkeys, the researchers found current materials used in medical implants, including ceramics, polymers, and even biocompatible hydrogels induce production of CSF1R proteins, which in turn promote development of scar tissue where the materials are implanted. Anderson’s lab is studying alginate as an implant material, a hydrogel made with natural substances found in algae that still induce an immune response and scar tissue.

In addition, the team discovered by blocking CSF1R proteins, they could stop the the build-up of scar tissue from implants of those materials. But the research uncovered another key finding: blocking CSF1R proteins stopped only the scar tissue build-up, not other functions of macrophages, such as healing wounds and fighting infections. These results suggest blocking CSF1R actions could make medical implants safer, while still preserving other helpful macrophage functions.

“We’re preventing the macrophages from toggling into an activated warning state where they sound the alarm for this massive immune response to show up,” says postdoctoral researcher and first author Joshua Doloff in a university statement. “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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