A new breakthrough study at the Karolinska Institutet in Sweden shows that type one diabetes can be prevented in mice.
Using diabetes-susceptible mice, the scientists formed three groups -- the treated group, the untreated group, and the macrophage group. The first group received macrophages that had been treated with a specific set of cytokines. The macrophage group received macrophages that had not been treated. The untreated group was left alone with no treatment.
In the end, only 25% of the mice who receive the cytokine treatment developed type one diabetes, compared to 83% in the other groups.
Essentially, the specially treated macrophages stopped their immune systems from destroying the pancreatic cells that produce insulin.
What is type one diabetes?
Type one diabetes occurs when the body's immune system attacks and eventually destroys the insulin-producing beta cells in the pancreas. The immune system destroys them because it sees them as harmful or as alien bodies that mean to hurt the body in some way. As beta cells are killed, insulin production dies down and the patient is forced to inject insulin.
These beta cells are found in theislets of Langerhansin the pancreas, making up about 80% of the cells in the islets. Healthy pancrei have almost one million islets. Insulin is only one of the hormones produced in that area and in the cells.
Experts have not yet determined what causes the immune system to suddenly attack beta cells.
Well then, what do we know about what causes diabetes?
Even though we don't know exactly what causes it, we do know that certain immune cells (macrophages) are highly active and play a major role in beta cell death. On the other hand, macrophages aren't always the killer; in fact, they can protect against inflammation and tissue damage.
We also know that cytokines, or signal molecules, are used for communication between macrophages. That is why the research team focused on cytokines: to learn more about what communication breakdowns cause the macrophages to kill too many beta cells.