Beta Cell Proliferation May Help Protect Against Type 1 Diabetes

Histology of human pancreatic tissue

In individuals with type 1 diabetes (T1D), the body’s immune system mistakenly attacks and destroys insulin-producing beta cells. For years, researchers have been looking at options for suppressing this immune system attack, as well as processes to replace beta cells or stimulate the body to produce more. A recent study by researchers at the Joslin Diabetes Center may have found a way to do both and increase protection against T1D.

Scientists found that by speeding up cell proliferation and flooding mouse models with beta cells, it stopped the immune system from destroying these cells. According to Dr. Rohit Kulkarni, HMS Professor of Medicine and Co-Section Head of Islet and Regenerative Biology at the Center, “We believe there are some alterations in the new beta cells where a number of cells being presented as autoantigens are reduced or diluted, and therefore, because of the slow presentation of the antigens, the number of autoreactive T cells are less pathogenic.” In addition, when these cells were transplanted into other mice, they appeared to have a greater resistance to stress, which could also help them to survive longer in adverse conditions.

Gaining a greater understanding of the role cell proliferation can play and determining when the ideal time to activate this process is could have a positive impact on improving protective factors against T1D. This process has not yet been tested in humans, and there would likely still be a need for some level of immune system suppression to manage lingering autoimmunity.

The Diabetes Research Connection (DRC) stays abreast of the latest developments regarding T1D and is interested to see how these findings impact future studies and treatment options for the disease. It is these types of projects that stimulate innovative studies from other researchers. The DRC provides critical funding to support early career scientists in pursuing novel, peer-reviewed research.


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