The story of type 1 diabetes begins in the pancreas, long seen as a battleground between insulin-producing beta cells and misguided immune defenders. Scientists have been searching for ways to detect this internal conflict early to prevent a lifelong disease that depletes the body’s insulin supplies.
Two new papers published Wednesday in Science Translational Medicine provide new clues about what happens in these beta cells before type 1 diabetes develops. Experiments in human cells and mouse models used biosensors and genetic analysis to uncover this pathway and detect possible ways to halt beta cell destruction.
In the first study, a team at Indiana University School of Medicine investigated how a particular immune cell involved in inflammation, known as the signaling cytokine interferon alpha, normally causes beta cells to produce other molecules that play a role in inflammation, cell proliferation, and cell death. These reactive oxygen species (ROS for short) can cause collateral damage. However, cells from type 1 diabetics did not contain ROS-producing beta cells, suggesting that they lack the cytokines that stimulate ROS production. The study authors speculated that this deficiency may serve as an early warning of beta cell decline in type 1 diabetes.
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