Preventing the Immune Response to Implanted Diabetes Devices

Preventing the Immune Response to Implanted Diabetes Devices

For people with diabetes, implanted medical devices can enable better treatment. A new study has shown that selectively blocking immune cells prevents scar tissue from developing around medical devices, which may improve their effectiveness .

JDRF has announced a report of one of the first studies to deeply examine the fundamentals of how the immune system interacts with implantable biomaterials. The study was conducted by researchers at MIT and Boston Children’s Hospital and was reported in the journal Nature Materials.

According to JDRF’s press release, tens of millions of people in the United States are living with implanted biomedical devices or devices that penetrate the skin. “By understanding how to target and prevent unnecessary immune responses to the materials used in medical devices, we can provide therapies that work more effectively and with fewer negative side effects,” said Aaron Kowalski, Ph.D., JDRF Chief Mission Officer. The new report, “Colony stimulating factor-1 receptor is a central component of the foreign body response to biomaterial implants in rodents and non-human primates,” could influence the future ability to prevent immune rejection of devices that treat type 1 diabetes.

Currently, devices like CGMs and infusion sets for insulin pumps must be changed regularly because the body’s immune response causes what’s known as a fibrotic cascade. Fibrosis is the thickening and scarring of connective tissue, usually as a result of injury. It can prevent an implanted device from interacting with the surrounding microenvironment, making it impossible for the device to sense glucose levels or effectively deliver insulin.

Fibrosis and immune responses have been an issue, too, for businesses like ViaCyte, a regenerative medicine company developing islet cell replacement therapy. Over the past 2 years, ViaCyte has implanted its devices of encapsulated cells under the skin of about 20 patients, without the use of immunosuppression drugs. In many recipients, although the cells have grown into insulin-producing beta cells, due to a fibrotic immune reaction on the device exterior, the cells often die after a few months.

A fibrotic immune reaction is different from the immune attack that originally destroys the patients’ beta cells and causes type 1 diabetes, but it can be equally damaging to the prospects of encapsulation. In other words, although the encapsulation protects the newly implanted beta cells from the autoimmune attack which originally caused diabetes, the device itself, like anything the body recognizes as foreign, can cause an immune reaction. In order to make encapsulation successful, researchers need to find a material, or a way for the body to accept the implanted device without the use of heavy immunosuppression, as immunosuppression itself may lead to a number of complications such as inhibiting wound healing. The ability to overcome the rejection of implanted medical devices without the use of broad-spectrum anti-inflammatory drugs could improve the lifespan and effectiveness of the devices, as well as the quality of patients’ lives.

The study reported in Nature Materials, conducted in rodents and non-human primates, found a significant increase in immune response from colony stimulating factor-1 receptor (CSFR-1). CSFR-1 is a component of the immune response. It’s a receptor for a protein called colony stimulating factor 1 (CSF1), which combats infection by “turning on” white blood cells that engulf foreign substances and cellular debris. Following implantation in the body of a number of biomaterial classes such as ceramic, polymer and hydrogel, led to an increase of CSF1R. Inhibiting CSF1R, however, led to a loss of fibrosis, but spared other necessary immune functions. This means that specifically targeting CSF1R improved biocompatibility and reduced the thickening and scarring of fibrosis without the need for broad immunosuppression.

“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,” said 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 (IMES), an affiliate at Boston Children’s Hospital, and the senior author of the study.

sources: JDRF, Nature

This research was supported by grants from JDRF, The Leona M. and Harry B. Helmsley Charitable Trust, the National Institutes of Health, and the Tayebati Family Foundation.

Jessica Apple
Jessica Apple

Jessica Apple grew up in Houston. She studied Bible and Ancient Near Eastern Studies at the University of Michigan, and completed an MA in the same field at the Hebrew University. She began to write and publish short stories while a student, and continues to write essays and fiction while raising her three sons (and many pets). Jessica’s work has appeared in The New York Times Magazine, The Financial Times Magazine, The Southern Review, The Bellevue Literary Review, Tablet Magazine, and elsewhere. She is the diabetes correspondent for The Faster Times. In 2009 she and her husband, both type 1 diabetics, founded A Sweet Life, where she serves as editor-in-chief. Jessica loves spending time with her sons, cooking with her husband, playing with her cats, reading, biking, drinking coffee, and whenever possible, taking a nap. Follow Jessica on Twitter (@jessapple)

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Rick Phillips
rick phillips
7 years ago

This is a nice start for this important research.

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