I tend to write mostly about type 2 diabetes, because that's what I know best. But lately, there have been some interesting developments that may lead to real cures in people with type 1, so I thought I'd switch gears for a bit and write about type 1.
Classic type 1 diabetes is an autoimmune disease. Your immune system attacks your beta cells and destroys them.
Normally, the body is able to distinguish between "self" and "nonself," and it leaves your own tissues alone. How it does this is incredibly complex, and no one understands it fully yet. Cells called regulatory T cells, often abbreviated to Treg, may play an important role.
For some reason, in some cases the system goes awry, and your immune system starts attacking your own cells. If it attacks the insulation around your nerve cells, you get multiple sclerosis. If it attacks your joints, you get rheumatoid arthritis. If it attacks your beta cells, you get type 1 diabetes.
Scientists can transplant beta cells into an animal or a human being with diabetes, but the immune system will just destroy those new beta cells the same way they destroyed the old ones, especially if the transplanted cells come from another person or from a different species. The transplantation protocol called the Edmonton protocol used a cocktail of immunosuppressive drugs to try to protect the transplanted beta cells. But most of them eventually failed anyway.
One problem with this type of approach is that it takes the beta cells from two cadavers to provide enough material for one patient. There simply aren't enough donors. A group in Israel led by Shimon Efrat has succeeded in getting beta cells to multiply in culture. This would greatly increase the supply. But human trials are not expected until 5 years or more.
Scientists are also trying to find out why the transplanted beta cells eventually stop producing insulin, as most did in the Edmonton protocol. One suggestion is that the accumulation of a protein called amyloid in the transplanted islets causes them to die. Amyloid deposits are found in most people with type 2 diabetes, and now researchers have found the same thing in transplanted beta cells in people with type 1. If they could figure out how to stop the formation of these deposits, it might benefit people with both types of diabetes.
Another approach is to encapsulate transplanted beta cells in structures that will let the relatively small insulin molecules out but won't let the larger antibodies in to destroy the cell. Scientists are working on different types of encapsulation, but so far none have been totally successful.
Another approach would be to get your own body to keep producing beta cells faster than they were being destroyed. Research in this area has focused on "stem cells," or the immature, unspecialized cells found mostly in embryos that are capable of differentiating into any cell type in the body.
However, the use of embryonic stem cells has become a political issue, and so scientists are looking for another approach. One is to try to get differentiated cells to revert to their embryonic stem cell state. Then the researchers would try to figure out how to stimulate the stem cells to differentiate into beta cells. Very recently, researchers at the University of North Carolina at Chapel Hill Medical School have announced that they have produced insulin-producing cells from skin cells. They first converted the skin cells into stem cells and then converted the stem cells into insulin-producing cells.