nPOD. Beta Cell Development, Differentiation & Regeneration

Exploring an islet-protective role for native pancreatic mesenchymal stromal cells in health and in type 1 diabetes

Our research aims to investigate how a group of adult stem cells, known as mesenchymal stem /stromal cells(MSCs), located in the pancreas may be involved in helping to protect people from developing type 1 diabetes(T1D). MSCs are found in most parts (tissues) of the body, including the pancreas, bone marrow, fat and kidney. When samples of these tissues are taken, MSCs can be isolated in the lab and when fed with appropriate nutrients will expand in number, so that we have enough MSCs that may be used therapeutically to treat inflammatory and autoimmune conditions, including T1D. Once isolated and expanded in this way we refer to these cells as exogenous MSCs, as opposed to endogenous/native MSCs that are found naturally in the tissue from which they were isolated.

Researchers in the diabetes field often refer to these exogenous MSCs as ‘Islet Helper’ cells. This is because experimental studies have shown that exogenous MSCs improve the ability of islet beta cells to produce insulin in response to increased sugar levels. Additionally, experimental studies have shown that exogenous MSCs can help to protect islet beta cells from immune attack and destruction. Clinical trials have shown that that exogenous bone marrow MSCs help to preserve the function of insulin producing islet beta cells in some individuals with newly diagnosed T1D, after infusion into the blood circulation.

Whilst we have established a lot about the function of exogenous MSCs, our understanding of endogenous/native MSCs located in the pancreas, with regards to their role in health and T1D is limited. We aim to determine whether the number, distribution and function of native pancreas MSCs is altered in T1D.We will determine whether native pancreas MSCs have a role in health to protect pancreatic islets from immune attack and destruction. These studies will provide scientific information on MSC-related changes inT1D, that we can target therapeutically to help delay or prevent the progression of diabetes. We will further establish whether there are differences in native pancreas MSC number, distribution and function in different subgroups of individuals with T1D, thus determining which subgroups are most likely to benefit from MSC-based therapeutic intervention.

Comments are closed.