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Diabetes Treatment

Could Peripheral T Helper Cells Be Linked to Type 1 Diabetes Risk?

Type 1 diabetes (T1D) is a complex disease. Researchers believe that both genetics and autoantibodies play a role in development of the disease. In individuals with T1D, the immune system mistakenly attacks and destroys insulin-producing beta cells in the pancreas. A new study has found that peripheral T helper cells may play a role in initiating this process.

The study showed that children with T1D, as well as those who were autoantibody-positive who developed the disease later on, both had an increase in the amount of peripheral T helper cells circulating in their blood. Researchers believe that much like follicular helper T cells, peripheral T helper cells may also be involved in activating B cells which target against proteins in pancreatic islet cells and contribute to the development of T1D.

The ability to identify children who are at increased risk for the disease due to genetics as well as the elevated presence of peripheral T helper cells may improve options for proactively monitoring and treating T1D. It could also support the development of new immunotherapies for the disease.

More research is necessary to better understand the role of this T-cell subset and how it impacts type 1 diabetes risk and development of the disease as well as how it could improve treatment or prevention options. Though not involved with this study, Diabetes Research Connection (DRC) follows the latest developments and advancements regarding type 1 diabetes understanding, treatment, and prevention.

DRC provides critical funding for early career scientists pursuing novel research studies related to the disease and hopes to one day find a cure. To learn more about current projects or how to help, visit http://diabetesresearchconnection.org.

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Role of the integrated stress response in type 1 diabetes pathogenesis
In individuals with type 1 diabetes (T1D), the insulin-producing beta cells are spontaneously destroyed by their own immune system. The trigger that provokes the immune system to destroy the beta cells is unknown. However, accumulating evidence suggest that signals are perhaps first sent out by the stressed beta cells that eventually attracts the immune cells. Stressed cells adapt different stress mitigation systems as an adaptive response. However, when these adaptive responses go awry, it results in cell death. One of the stress response mechanisms, namely the integrated stress response (ISR) is activated under a variety of stressful stimuli to promote cell survival. However, when ISR is chronically activated, it can be damaging to the cells and can lead to cell death. The role of the ISR in the context of T1D is unknown. Therefore, in this DRC funded study, we propose to study the ISR in the beta cells to determine its role in propagating T1D.
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