Could islet helper cells in the pancreas delay or prevent type 1 diabetes?

We’re funding Dr Rebecca Dewhurst-Trigg at the University of Exeter to investigate how mesenchymal stem/stromal cells (MSCs) in the pancreas, also known as islet helper cells, may be involved in stopping harmful immune cells attacking insulin-making beta cells. This could lead to new ways to protect beta cells which could help delay or prevent type 1 diabetes (T1D).

What are pancreatic islets?

Islets, short for islets of Langerhans, are cluster of cells in the pancreas. Islets contain the insulin-making beta cells which are destroyed in T1D. They also contain cells that release other hormones, like glucagon. The cells inside the islets are protected by a barrier around the outside, called the basement membrane. This membrane is weakened in T1D meaning harmful immune cells can enter the islet and attack the beta cells within it.

What are mesenchymal stromal cells?

MSCs are found in most parts of the body, such as the pancreas, bone marrow, fat tissue and kidneys. MSCs in the pancreas make lots of helpful products including the building blocks of the islet basement membrane. Rebecca’s initial research has shown that more MSCs are wrapped around the basement membrane of islets that still have beta cells, compared to islets where the beta cells have been destroyed.

Why are Breakthrough T1D funding this project?

Although previous research has helped us understand how MSCs work, we know a lot less about how they support the basement membrane of islets to protect beta cells against immune attack. By studying how MSCs make the basement membrane building blocks, Rebecca aims to see whether they are involved in maintaining or repairing the protective islet border which could lead to new ways to protect beta cells.

Rebecca said:

“Our research will investigate how MSCs might help protect insulin-producing beta cells from immune cell attack in type 1 diabetes. The protective border around islets, called the basement membrane, is weakened in type 1 diabetes which leaves beta cells vulnerable to immune cell attack. MSCs could produce the components, or building blocks, of the islet basement membrane and may play a role in supporting and repairing this protective barrier around islets. By studying how MSCs produce the basement membrane building blocks, we aim to determine whether they are involved in maintaining or repairing this protective islet border. This research may lead to new ways to protect beta cells, potentially helping to delay or prevent the progression of type 1 diabetes and improve the success of beta cell replacement therapies by better protecting transplanted beta cells.”

What will Rebecca do in this project?

In this project, Rebecca will run several experiments on human MSCs outside of the body in a laboratory to tell us whether MSCs are different in T1D. Rebecca will expose MSCs to conditions that reflect what happens in the body in T1D and test how MSCs survive and produce the islet basement membrane building blocks. Rebecca will also test how the protective barrier around islets stops immune cells from entering and attacking the beta cells within.

How will this project help people with T1D?

Rebecca’s project will provide scientific information on MSC-related changes in T1D that could be targeted with a treatment to help delay or prevent T1D. Findings from Rebecca’s project could also help protect beta cells that have been replaced through islet transplants. Islet transplants are where islets taken from organ donors are put into people living with T1D to give them the ability to make insulin again.

Is Breakthrough T1D funding any other research like this?

We are also funding Dr Chloe Rackham at the University of Exeter to investigate how MSCs may be different in people with T1D. Using a microscope and imaging techniques, Chole is studying pancreas samples from newly diagnosed children to find out how MSCs change in T1D. Chole’s research will tell us whether MSCs play a part in stopping the immune system from destroying beta cells and causing T1D.