Type 1A Diabetes develops because the body mistakenly identifies insulin-producing cells (beta cells) as being foreign, or "non-self." The immune system targets and ultimately destroys the beta cells, resulting in an absence of insulin and the subsequent diagnosis of diabetes. This autoimmune process is thought to smolder for years, and there are individuals at risk of developing diabetes who do not yet have the diagnosis.
During the "prodrome," or prior to the time of diagnosis, it is speculated that the regulatory T cells are unable to control cytotoxic T cells directed against self proteins.
CD4 and CD8 T cells coordinate to attack and destroy insulin-producing cells (beta cells). At the same time, B cells are making antibodies against beta cell proteins.
There may be some beta cell re-formation (by cell division or by new cell formation) that replaces the destroyed cells. But over the years, the net destruction is greater than the replacement. When the number of beta cells is reduced by approximately 80%, the body is unable to secrete enough insulin, the blood sugar rises and clinical diabetes is diagnosed. The diagnosis of diabetes is based on an elevated blood sugar.
This prolonged development period prior to the diagnosis of diabetes has several implications:
- At-risk individuals may be identified.
- At-risk individuals will still have significant beta cell function.
- What is happening in the autoimmune process on a cellular and molecular basis can be studied.
- If we know how to interrupt or stop the process, we may be able to delay and prevent progression to diabetes.