The story of type 1 diabetes begins in the pancreas, long seen as a battleground between insulin-producing beta cells and misdirected immune defenders. Scientists have been searching for ways to spot this internal warfare early enough to prevent a lifelong disease that depletes the body’s source of insulin.
Two new papers published Wednesday in Science Translational Medicine offer new clues to what happens in these beta cells before type 1 diabetes emerges. Experiments in human cells and in mouse models used biosensors and genetic analyses to illuminate this pathway and detect possible ways to halt beta-cell destruction.
In the first study, a team from the Indiana University School of Medicine explored how certain immune cells involved in inflammation, known as signaling cytokine interferon-alpha, normally trigger beta cells to produce other molecules that play a role in inflammation, cell proliferation, and cell death. These reactive oxygen species, ROS for short, sometimes cause collateral damage. But cells from patients with type 1 diabetes did not have ROS-producing beta cells, suggesting they lacked the cytokines that stimulate their ROS production. That dearth might be useful in flagging the decline of beta cells early on in type 1 diabetes, the study authors surmised.
