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Red Blood Cells

Improving PD-L1 Levels to Treat Type 1 Diabetes

A major obstacle that researchers face in treating type 1 diabetes (T1D) is the body’s own immune system. In individuals with T1D, the immune system destroys insulin-producing beta cells whether naturally occurring or introduced through novel therapeutic approaches. The use of anti-rejection drugs to protect newly injected or created cells can be hard to the body and contribute to undesirable side effects.

However, researchers at Boston Children’s Hospital are studying a new approach to treating – and potentially curing – T1D. They found that in individuals with T1D have a deficiency of PD-L1, a protein that helps prevent autoimmune reactions by binding to PD-1 receptors. By treating blood stem cells using gene therapy or a cocktail of small molecules, they were able to increase PD-L1 production. In turn, this helped to reverse hyperglycemia and better manage blood sugar levels.

In an experiment using mice with diabetes, “almost all the mice were cured of diabetes in the short term, and one-third maintained normal blood sugar levels for the duration of their lives.” In addition, the risk of adverse events is practically eliminated since the therapy uses the patients’ own cells. Though immunotherapies have been used before in an effort to treat T1D, they have not been targeted specifically for diabetes, whereas in this study, they are.

The research team has already met with the U.S. Food and Drug Administration for a pre-investigational new drug meeting regarding the combination of small-molecules used during the mouse trials in order to begin the approval process for human clinical trials.

This is an exciting step toward advancing treatment options for type 1 diabetes and potentially reversing the disease. More research is needed to determine how long the effects last and how often treatment would be needed.

The Diabetes Research Connection (DRC) is interested to see how the study progresses in the future and what it could mean for individuals living with type 1 diabetes. Though not involved with this particular project, the DRC supports early career scientists in pursuing novel research studies geared toward preventing, treating, and curing T1D, as well as improving quality of life for those living with the disease. Learn more about these researchers and their projects by visiting 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.
Wearable Skin Fluorescence Imaging Patch for the Detection of Blood Glucose Level on an Engineered Skin Platform
zhang
A Potential Second Cure for T1D by Re-Educating the Patient’s Immune System
L Ferreira
Validating the Hypothesis to Cure T1D by Eliminating the Rejection of Cells From Another Person by Farming Beta Cells From a Patient’s Own Stem Cells
Han Zhu
Taming a Particularly Lethal Category of Cells May Reduce/Eliminate the Onset of T1D
JRDwyer 2022 Lab 1
Can the Inhibition of One Specific Body Gene Prevent Type 1 Diabetes?
Melanie
Is Cholesterol Exacerbating T1D by Reducing the Functionality and Regeneration Ability of Residual Beta Cells?
Regeneration Ability of Residual Beta Cells
A Call to Question… Is T1D Caused by Dysfunctionality of Two Pancreatic Cells (β and α)?
Xin Tong
Novel therapy initiative with potential path to preventing T1D by targeting TWO components of T1D development (autoimmune response and beta-cell survival)
flavia pecanha